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1.
Med. clín (Ed. impr.) ; 152(11): 425-430, jun. 2019. ilus, graf
Artigo em Inglês | IBECS | ID: ibc-183902

RESUMO

Introduction: Melanoma is the most dangerous skin cancer with high metastasis rate and mortality. Although the emergence of immunotherapy has brought hope for treatment, the mortality rate of melanoma is still increasing year by year. The underlying mechanism of melanoma tumor progression and metastasis is urgently needed to be clarified. Recently chemokines have been found to play an important role in tumor progression in addition to their immunocytochemical chemotaxis. Methods: In this study, human melanoma cell lines A375 and M14 were treated with SCH-527123, a small molecule antagonist of CXCR1 and CXCR2. The effects of treatment with SCH-527123 on melanoma cell proliferation, migration and invasion were evaluated in vitro by CCK-8, colony formation and transwell assays. Apoptosis was also detected by flow cytometry staining with annexin V and propidium iodide (PI). The molecular mechanisms of antagonist mediated were detected by western blot. Results: The results showed that SCH-527123 inhibited the proliferation, migration and invasion of melanoma cell lines and promoted apoptosis. The expression of CXCR1 and CXCR2 was downregulated after treatment with SCH-527123. PI3K/AKT pathway and downstream signaling were also inhibited at molecular level owing to treated with SCH-527123. Conclusion: In conclusion, our study demonstrated that SCH-527123, a small-molecule antagonist for CXCR1 and CXCR2 inhibited cell proliferation, migration and invasion in melanoma via PI3K/AKT pathway


Introducción: El melanoma es el cáncer de piel más peligroso, con una alta tasa de metástasis y mortalidad. Aunque la inmunoterapia ha traído esperanza para el tratamiento, la tasa de mortalidad del melanoma sigue aumentando año tras año. Es de crucial importancia aclarar el mecanismo subyacente de la evolución y la metástasis del melanoma. Recientemente se ha descubierto que las quimiocinas juegan un importante papel en la evolución tumoral. Métodos: En el presente estudio, las líneas celulares de melanoma humano A375 y M14 se trataron con SCH-527123, un inhibidor de molécula pequeña de CXCR1 y CXCR2. Los efectos del tratamiento con SCH-527123 sobre la proliferación, migración e invasión de células de melanoma se evaluaron in vitro mediante CCK-8, formación de colonias y ensayos Transwell. También se detectó apoptosis mediante citometría de flujo con tinción con anexina V y yoduro de propidio (PI). Los mecanismos moleculares del antagonista fueron detectados por Western blot. Resultados: Los resultados mostraron que SCH-527123 inhibió la proliferación, migración e invasión de líneas celulares de melanoma y promovió la apoptosis. La expresión de CXCR1 y CXCR2 disminuyó después del tratamiento con SCH-527123. La vía de señalización de la PI3K/AKT también se inhibió a nivel molecular debido a que se trataron con SCH-527123. Conclusión: Nuestro estudio demostró que SCH-527123, un inhibidor de molécula pequeña para CXCR1 y CXCR2 inhibió la proliferación celular, la migración y la invasión del melanoma a través de la vía PI3K/AKT


Assuntos
Humanos , Receptores de Interleucina-8A/agonistas , Receptores de Interleucina-8B/agonistas , Invasividade Neoplásica , Melanoma/patologia , Apoptose/efeitos dos fármacos , Proteínas Proto-Oncogênicas c-akt/efeitos dos fármacos , Antineoplásicos/farmacologia , Proliferação de Células , Movimento Celular , Células Tumorais Cultivadas , Transdução de Sinais
2.
Cir. plást. ibero-latinoam ; 45(2): 107-114, abr.-jun. 2019. ilus, graf
Artigo em Espanhol | IBECS | ID: ibc-184218

RESUMO

Introducción y objetivo. Las células madre son candidatas terapéuticas para una amplia gama de enfermedades. Resultan de gran interés en Cirugía Plástica para el tratamiento de heridas crónicas, transferencia de tejido adiposo y colgajos. El objetivo de este estudio es describir el método de aislamiento, cultivo y caracterización de células madre derivadas de tejido adiposo y cómo estas pueden precondicionarse con hipoxia y generar cambios in vitro en su capacidad proliferativa y migratoria. El trabajo es un complemento didáctico a otro publicado por nosotros en esta misma revista utilizando esta metodología en comparación al grupo de retardo de colgajo y grupo control en colgajos cutáneos aleatorizados en ratas. Métodos. Obtuvimos las células madre de tejido graso ínguino-abdominal de ratas adultas: 10 en el grupo de células madre derivadas de tejido adiposo y otras 10 en el grupo de células madre derivadas de tejido adiposo precondicionadas con hipoxia (2% O2 y 5% CO2). Realizamos análisis morfológico directo y con inmunofluorescencia con el marcador vimentina y CD90 y estudio de proliferación y migración celular in vitro. Resultados: Utilizamos en promedio 1.64 +/- 1.13 gr de tejido adiposo en el grupo sin precondicionamiento y 0.93 +/- 0.34 gr en el grupo con precondicionamiento con hipoxia para el aislamiento. Las células madre derivadas de tejido adiposo precondicionadas con hipoxia presentaron un aumento de la capacidad migratoria a las 24 horas de 2.44 +/- 0.85 mm frente a 2.24 +/- 0.82 mm (p ≤ 0.01) y proliferativa 5.42 x105 +/- 1.03 x105 céls/ml frente a 3.26 x105 +/- 8.61 x104 céls/ml) (p ≤ 0.001) de forma significativa en comparación a las sin precondicionamiento. Conclusiones. Describimos en detalle un método de precondicionamiento de células madre mediante hipoxia. Logramos potenciar el efecto de las células madre aumentando en forma significativa su capacidad migratoria y proliferativa de forma precoz


Background and objective. Stem cells are therapeutic candidates for a wide range of diseases. They are of great interest in Plastic Surgery for the management of chronic wounds, adipose tissue transfer and flaps. The objective of this study is to describe the method of isolation, culture and characterization of stem cells derived from adipose tissue and how these can be preconditioned with hypoxia and generate in vitro changes in their proliferative and migratory capacity. This study is a didactic supplement to a paper published by us in this same journal using this methodology in comparison to the group of flap delay and control group in skin flaps randomized in rats. Methods. Stem cells were obtained from inguinal-abdominal fatty tissue of adult rats: 10 in the group of stem cells derived from adipose tissue and another 10 in the group of stem cells derived from adipose tissue preconditioned with hypoxia (2% O2 and 5% CO2). Direct morphological analysis was carried out and with immunofluorescence (vimentin and CD90 marker). Study proliferation and in vitro cell migration was performed. Results. An average of 1.64 +/- 1.13 gr of adipose tissue of the inguinoabdominal area was used in the group of stem cells without preconditioning and 0.93 +/- 0.34 gr. in the group with hypoxic preconditioning for the isolation. Stem cells derived from adipose tissue preconditioned with hypoxia showed an increase in migratory capacity at 24 hours of 2.44 +/- 0.85 mm v/s 2.24 +/- 0.82 mm (p ≤ 0.01) and proliferative of 5.42 x105 +/- 1.03 x105 cells / ml v/s 3.26 x 105 +/- 8.61 x104 cells / ml) (p ≤0.001) significantly compared to those without preconditioning. Conclusions. A method of preconditioning stem cells by hypoxia is described in detail. It is possible to enhance the effect of the stem cells, significantly increasing their early migratory and proliferative capacity


Assuntos
Animais , Masculino , Ratos , Células-Tronco/citologia , Tecido Adiposo/citologia , Hipóxia/veterinária , Tecido Adiposo/enzimologia , Movimento Celular , Ratos Sprague-Dawley , Técnicas In Vitro/instrumentação , Tecido Adiposo/metabolismo , Imuno-Histoquímica , Proliferação de Células , Imunofluorescência , Neovascularização Fisiológica
3.
Allergol. immunopatol ; 47(2): 185-193, mar.-abr. 2019. ilus, graf
Artigo em Inglês | IBECS | ID: ibc-180808

RESUMO

Introduction: Asthma is a chronic inflammatory disease of the airways. In this study, we evaluated the anti-inflammatory effects of myrtenol on the inflammatory indices in the pulmonary parenchyma and airways and on the inflammatory and oxidative indices of the bronchoalveolar lavage fluid (BALF) of asthmatic rats. Methods: The allergic asthma was induced by sensitization (two weeks) followed by the inhalation of ovalbumin (four weeks). Animals were divided into two main groups: (1) Histopathology, and (2) measurement of inflammatory and oxidative biomarkers in the BALF. Each main group was subdivided into four subgroups: Control, Asthma, Asthma+Dexamethasone and Asthma + Myrtenol. (-)-Myrtenol (50 mg/kg) or Dexamethasone (2.5 mg/kg) was administered intraperitoneally once a day for one week, at the end of the inhalation period. On day 50, lung histopathologic parameters and inflammatory indices in BALF including INF-gamma, IL-10, IL-1Beta, and TNF-alfa and oxidative stress biomarkers (MDA, SOD, and GPX) were measured. Result: In the Asthma group, leukocyte infiltration, the thickness of smooth muscle and epithelium of airways wall and the number of goblet cells increased. Myrtenol reduced all of the above-mentioned indices except the epithelium thickness. It also inhibited the increase in BALF IL-1Beta, TNF-alfa and MDA and increased the levels of INF-gamma, IL-10 and SOD. Conclusion: Our results suggest that myrtenol reduced damage caused by experimental asthma by reducing the inflammatory indices, normalizing the level of interleukins and balancing oxidative stress in the lungs. It also prevented airway remodeling. Myrtenol may be suggested as a potent herbal medicine for the treatment of allergic asthma


No disponible


Assuntos
Humanos , Animais , Masculino , Remodelação das Vias Aéreas/efeitos dos fármacos , Anti-Inflamatórios/uso terapêutico , Asma/tratamento farmacológico , Células Caliciformes/patologia , Leucócitos/imunologia , Pulmão/imunologia , Mucosa Respiratória/patologia , Monoterpenos/uso terapêutico , Movimento Celular , Células Cultivadas , Citocinas/metabolismo , Modelos Animais de Doenças , Mediadores da Inflamação/metabolismo , Ratos Wistar , Mucosa Respiratória/efeitos dos fármacos
4.
Rev. osteoporos. metab. miner. (Internet) ; 11(1): 12-18, mar. 2019. graf
Artigo em Espanhol | IBECS | ID: ibc-184080

RESUMO

La fuerza mecánica es importante para el modelado, el remodelado y la regeneración ósea; estimula a los osteocitos provocando una alteración en la producción y secreción de moléculas de señalización que regulan la actividad de los osteoblastos y los osteoclastos. El objetivo del presente estudio fue evaluar el efecto del medio condicionado de células osteocíticas de ratón estimuladas mecánicamente sobre la capacidad proliferativa y migratoria de células mesenquimales y células óseas. Para ello, se analizó la proliferación y migración de las células preosteoblásticas de ratón, células mesenquimales preadiposas humanas y macrófagos de ratón en presencia del medio condicionado de las células osteocíticas, tras 6 y 24 horas después de ser sometidas a un estrés mecánico de 10 dinas/cm2 por flujo de fluido (FF) durante 10 minutos. Se encontró que la migración de células preosteoblásticas aumentó significativamente en presencia de medios condicionados de células osteocíticas con respecto al grupo control estático (SC) (SC=12,63±5,44; FF6h=23,03±11,57; FF24h=29,72±15,76; p<0,0001). De la misma manera, las células preadiposas también incrementaron significativamente su migración en presencia de dichos medios condicionados (SC=11,48±4,75; FF6h=18,43±9,94; FF24h=18,80±10,03; p≤0,0007). Sin embargo, la migración de los macrófagos disminuyó en presencia del medio condicionado recogido a las 24 horas con respecto al grupo control estático (SC=69±22,71; FF24h=26,57±5,47; p<0,0001). Estos efectos se asociaron con la disminución de la expresión proteica de ciertas quimioquinas, como la proteína quimiotáctica de monocitos de tipo I (SC=0,25±0,06; FF24h=0,09±0,005; p=0,0262), la proteína del grupo I de alta movilidad (SC=0,25±0,04; FF24h=0,15±0,05; p=0,0159) y la proteína reguladora de la activación de linfocitos T y monocitos (SC=3,29±0,88; FF6h=1,33±1,09; FF24h=0,97±0,66; p≤0,0314), por parte de los osteocitos en presencia de estímulo mecánico con respecto al grupo control estático. En conclusión, este estudio in vitro demuestra que la mecanotransducción de los osteocitos potencia el reclutamiento de osteoblastos y células mesenquimales preadiposas mientras que reduce la migración de los macrófagos


Mechanical force is important for modeling, remodeling and bone regeneration. It stimulates the osteocytes, causingan alteration in the production and secretion of signaling molecules that regulate osteoblast and osteoclast activity.The present study aims to evaluate the effect of the conditioned medium of mechanically stimulated mouse osteocyticcells on the proliferative and migratory capacity of mesenchymal cells and bone cells. For this, the proliferation andmigration of mouse pre‐osteoblastic cells, human pre‐adult mesenchymal cells and mouse macrophages in the pre‐sence of the conditioned medium of osteocytic cells were analyzed, after 6 and 24 hours after being subjected to amechanical stress of 10 dynes/cm2by fluid flow (FF) for 10 minutes. The migration of pre‐osteoblastic cells has beenfound to increase significantly in the presence of conditioned media of osteocytic cells compared to the static controlgroup (SC)(SC=12.63±5.44, FF6h=23.03±11.57, FF24h=29.72±15.76, p<0.0001). In the same way, the pre‐adipose cellsalso significantly increased their migration in the presence of this conditioned media (SC=11.48±4.75, FF6h=18.43±9.94,FF24h=18.80±10.03; p≤0.0007). However, macrophage migration decreased in the presence of the conditioned mediumcollected at 24 hours with respect to the static control group (SC=69±22.71, FF24h=26.57±5.47, p<0.0001). Theseeffects were associated with decreased protein expression of certain chemokines, such as the monocyte chemotacticprotein type I (SC=0.25±0.06, FF24h=0.09±0.005, p=0.0262), the protein of group I of high mobility (SC=0.25±0.04,FF24h=0.15±0.05, p=0.0159) and the regulatory protein of the activation of T lymphocytes and monocytes(SC=3.29±0.88, FF6h=1.33±1.09, FF24h=0.97±0.66, p≤0.0314), by the osteocytes in the presence of mechanical stimu‐lation with respect to the static control group. In conclusion, this in vitro study demonstrates that osteocyte mechano‐transduction enhances recruitment of osteoblasts and pre‐adipose mesenchymal cells while reducing the migration ofmacrophages


Assuntos
Humanos , Mecanotransdução Celular/fisiologia , Osteócitos/fisiologia , Proliferação de Células , Movimento Celular , Células-Tronco Mesenquimais/fisiologia , Células Cultivadas
5.
J. physiol. biochem ; 74(3): 491-501, ago. 2018. graf, ilus
Artigo em Inglês | IBECS | ID: ibc-179002

RESUMO

Glycosylation of cell surface proteins regulates critical cellular functions, including invasion and metastasis in cancer cells. Emerging evidence has shown that microRNAs (miRNAs) are involved in regulating both the glycosylation modifications on cell surface and the progression of cancer. In this study, we investigated the role of miR-9 in alfa -2,6-linked sialylation and the metastasis of mouse hepatocellular carcinoma (HCC). According to array-based miRNA expression profiling data of HCC cell lines Hepa1-6, Hca-P, and Hca-F with different lymphatic metastatic capacities, reverse correlation was found between miR-9 expression levels and the metastatic potential in these HCC cells. Additionally, Beta-galactoside alfa -2,6-sialyltransferase 1 (St6gal1) expression level is associated negatively with miR-9 and positively with metastatic potential. Bioinformatics analysis indicated that miR-9 could target St6gal1, which was verified by luciferase reporter assays. miR-9 overexpression reduced expression of St6gal1, which subsequently suppressed HCC cells metastatic potential. Moreover, upregulation of miR-9 could inhibit integrin-Beta1/FAK-mediated cell motility and migration signaling in mouse HCC cells. Together, our results suggest that miR-9 could act as a tumor suppressor and regulate mouse HCC cells migration and invasion by inhibiting the alfa-2,6-linked sialylation. This finding may provide insight into the relationship between abnormal miRNA expression and aberrant cell surface glycosylation during tumor lymphatic metastasis


No disponible


Assuntos
Humanos , Animais , Camundongos , Carcinoma Hepatocelular/genética , Regulação Neoplásica da Expressão Gênica , Neoplasias Hepáticas/genética , Neoplasias Hepáticas Experimentais/genética , MicroRNAs/genética , Sialiltransferases/genética , Sequência de Bases , Carcinoma Hepatocelular/metabolismo , Carcinoma Hepatocelular/patologia , Movimento Celular , Linhagem Celular Tumoral , Biologia Computacional , Quinase 1 de Adesão Focal , Glicosilação , Luciferases , Metástase Linfática
6.
Clin. transl. oncol. (Print) ; 20(6): 775-784, jun. 2018. ilus, tab, graf
Artigo em Inglês | IBECS | ID: ibc-173627

RESUMO

Purpose: Colorectal cancer (CRC) is one of the most widely diagnosed cancers in men and women worldwide. With the advancement of next-generation sequencing technologies, many studies have highlighted the involvement of long non-coding RNAs (lncRNAs) in cancer development. Growing evidence demonstrates that lncRNAs play crucial roles in regulating gene and protein expression and are involved in various cancers, including CRC. The field of lncRNAs is still relatively new and a lot of novel lncRNAs have been discovered, but their functional roles are yet to be elucidated. This study aims to characterize the expression and functional roles of a novel lncRNA in CRC. Method: Several methods were employed to assess the function of LOC285629 such as gene silencing, qPCR, proliferation assay, BrdU assay, transwell migration assay, ELISA and protein profiler. Results: Via in silico analyses, we identified significant downregulation of LOC285629, a novel lncRNA, across CRC stages. LOC285629 expression was significantly downregulated in advanced stages (Stage III and IV) compared to Stage I (Kruskal-Wallis Test; p = 0.0093). Further in-house validation showed that the expression of LOC285629 was upregulated in colorectal cancer tissues and cell lines compared to the normal counterparts, but was downregulated in advanced stages. By targeting LOC285629, the viability, proliferative abilities, invasiveness and resistance of colorectal cancer cells towards 5-fluorouracil were reduced. It was also discovered that LOC285629 may regulate cancer progression by targeting several different proteins, namely survivin, BCL-xL, progranulin, PDGF-AA, enolase 2 and p70S6 K. Conclusion: Our findings suggest that LOC285629 may be further developed as a potential therapeutic target for CRC treatment


No disponible


Assuntos
Humanos , Masculino , Feminino , Pessoa de Meia-Idade , Neoplasias Colorretais/patologia , RNA Longo não Codificante/genética , Resistencia a Medicamentos Antineoplásicos/genética , Regulação Neoplásica da Expressão Gênica/genética , Neoplasias Colorretais/tratamento farmacológico , Neoplasias Colorretais/genética , Movimento Celular/genética , Proliferação de Células/genética , Antimetabólitos Antineoplásicos/farmacocinética , Fluoruracila/farmacocinética
7.
Clin. transl. oncol. (Print) ; 19(9): 1133-1140, sept. 2017. tab, graf, ilus
Artigo em Inglês | IBECS | ID: ibc-165215

RESUMO

Purpose. The objective of the study was to investigate the role of microRNA-9 (miR-9) targeting forkhead box O1 (FOXO1) in the proliferation, migration, and invasion of breast cancer cells. Methods. Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to determine the expressions of miR-9 and FOXO1 mRNA in breast cancer tissues, normal breast tissues, breast cancer cell lines, and normal breast epithelial cells. After the up-regulation of miR-9 expression, qRT-PCR and Western blotting were used to determine the expression of FOXO1. The luciferase reporter gene assay was used to validate the target gene. The CCK-8 assay, scratch-wound healing assay, and Transwell invasion assay were used to investigate the changes in the proliferation, migration, and invasion of breast cancer cells, respectively. Results. MicroRNA-9 expression was significantly up-regulated in breast cancer tissues and breast cancer cell lines when compared with normal breast tissues and normal breast epithelial cells (both P < 0.05). FOXO1 mRNA and protein expressions were substantially down-regulated in breast cancer tissues and breast cancer cell lines when compared with normal breast tissues and normal breast epithelial cells (both P < 0.05). There can be a negative correlation between miR-9 and FOXO1 mRNA in breast cancer. Luciferase reporter gene assay indicated that miR-9 can down-regulate FOXO1 expression at a post-transcriptional level through binding specifically to FOXO1 3′UTR. The results of CCK-8 assay, scratch-wound healing assay, and Transwell invasion assay revealed that the inhibition of miR-9 can suppress MCF7 cell proliferation, migration, and invasion. Additionally, the expression of miR-9 increased significantly whilst that of FOXO1 decreased substantially as the disease progressed (P < 0.05). Conclusions. Our study provides evidence that miR-9 can promote the proliferation, migration, and invasion of breast cancer cells via down-regulating FOXO1 (AU)


No disponible


Assuntos
Humanos , Feminino , MicroRNAs/análise , Proliferação de Células , Movimento Celular , Neoplasias da Mama/diagnóstico , Proteínas Oncogênicas v-fos/análise , Mama/citologia , Mama/patologia , Western Blotting/métodos , Transfecção , Reação em Cadeia da Polimerase , Luciferases/análise , Luciferases/genética
8.
Clin. transl. oncol. (Print) ; 19(5): 562-570, mayo 2017. graf
Artigo em Inglês | IBECS | ID: ibc-162189

RESUMO

Objective. Recent studies have identified Engrailed-2 (EN-2), a homeobox-containing transcription factor, as a candidate oncogene in prostate cancer (PC). Therapeutic targeting on EN-2, however, is limited because the mechanism underlying EN-2 overexpression in prostatic cancer cells is unknown. This study was to investigate the potential regulatory role of miR-33a on EN-2 expression and explore this signaling axis in ability of prostate cancer survival and metastasis. Methods. The relative expression of miR-33a and EN-2 in paired prostate cancer tissue and adjacent normal tissue as well as in prostate cancer cell lines, PC3 and DU145, was determined using quantitative real-time PCR or western blot, respectively. Cells survival, migration and invasion were evaluated by assays of MTT, TUNEL and Boyden chamber assays, respectively. Direct regulation of EN-2 by miR-33a was examined by luciferase reporter assay. Results. The data showed that miR-33a was upregulated and EN-2 was downregulated in both prostate cancer tissue and prostate cancer cells. miR-33a overexpression suppresses prostate cancer cell survival and metastasis. miR-33a can directly act on EN-2 expression by binding to 3′UTR of its mRNA. Also, miR-33a negatively regulated EN-2 mRNA and protein expression. In pcDNA-EN-2 and miR-33a mimic co-transfected PC3 and DU145 cells, EN-2 overexpression reverses the anti-cell survival and metastasis actions of miR-33a overexpression. The pivotal role of miR-33a in inhibiting prostate tumor growth was confirmed in xenograft models of prostate cancer. Conclusion. Our data suggest that the functional interaction of miR-33a and EN-2 is involved in tumorigenesis of prostate cancer. Also in this process EN-2 serves as a negative responder for miR-33a (AU)


No disponible


Assuntos
Humanos , Masculino , Neoplasias da Próstata/complicações , Neoplasias da Próstata/patologia , Metástase Neoplásica/fisiopatologia , RNA Mensageiro/genética , Proteína de Suscetibilidade a Apoptose Celular/genética , Movimento Celular/genética , Biomarcadores Tumorais/genética , Neoplasias da Próstata/genética , Reação em Cadeia da Polimerase/tendências , RNA Mensageiro/metabolismo , Western Blotting , Luciferases/análise , Análise de Variância , Repressão Epigenética/genética , Proto-Oncogenes/genética , Proteínas Oncogênicas/genética
9.
Clin. transl. oncol. (Print) ; 19(1): 125-133, ene. 2017. tab, graf
Artigo em Inglês | IBECS | ID: ibc-159127

RESUMO

Purpose. Tumor expansion is dependent on neovascularization, a process that requires sustained new vessel formation. Although the critical role of angiogenesis by endothelial sprouting in this process, controversy still prevails on whether angiogenesis involving bone marrow-derived endothelial cells, does contribute to this process. This study aims to evaluate the recruitment of bone marrow-derived cells by the melanoma tumor, including endothelial cells, and if they contribute to angiogenesis. Methods. A chimeric mouse model of GFP bone marrow was used to induce melanoma tumors derived from murine B16-F10 cell line. These tumors were evaluated for the presence of myeloid cells (CD11b), T lymphocytes (CD3, CD4 and CD8) and endothelial cells (VEGFR2 and CD31) derived from bone marrow. Results. Mice transplanted with GFP+ cells showed significant bone marrow chimerism (90.9 ± 0.87 %) when compared to the GFP transgenic mice (90.66 ± 2.1 %, p = 0.83) demonstrating successful engraftment of donor bone marrow stem/progenitor cells. Analysis of the murine melanoma tumor showed the presence of donor cells in the tumors (3.5 ± 1.7 %) and interestingly, these cells represent endothelial cells (CD31+ cells; 11.5 ± 6.85 %) and myeloid cells (CD11b+ cells; 80 ± 21 %), but also tumor-infiltrating lymphocytes (CD8+ T cells, 13.31 ± 0.2 %; CD4+ T-cells, 2.1 ± 1.2 %). Examination of the tumor endothelium by confocal microscopy suggests the presence of donor CD31+/GFP+ cells in the wall of some blood vessels. Conclusion. This study demonstrates that bone marrow-derived cells are recruited by the murine melanoma tumor, with myeloid cells and CD4 and CD8 T lymphocytes migrating as antitumor immune response, and endothelial cells participating of the tumor blood vessels formation (AU)


No disponible


Assuntos
Animais , Masculino , Feminino , Camundongos , Neoplasias do Tronco Encefálico/epidemiologia , Medula Óssea/patologia , Células da Medula Óssea/patologia , Melanoma/patologia , Neoplasias de Tecido Vascular/complicações , Neoplasias de Tecido Vascular/diagnóstico , Movimento Celular/fisiologia , Transplante de Medula Óssea/métodos , Molécula-1 de Adesão Celular Endotelial a Plaquetas/análise , Modelos Animais , Neoplasias do Tronco Encefálico/sangue , Células da Medula Óssea , Células Endoteliais , Células da Medula Óssea/efeitos da radiação , Células Endoteliais/patologia , Células Endoteliais , Neovascularização Patológica/terapia , Antígenos CD4/análise , Antígeno CD11b/análise
10.
J. physiol. biochem ; 72(4): 583-592, dic. 2016. graf, ilus
Artigo em Inglês | IBECS | ID: ibc-168366

RESUMO

Age-related macular degeneration (AMD) is the leading cause of blindness in the elderly. Late-stage AMD is characterized by choroidal neovascularization (CNV). miR-93 appears to play a role in regulating vascular endothelial growth factor-A (VEGF-A), a known factor involved in neovascularization. Understanding its biological significance might enable development of therapeutic interventions for diseases like AMD. We aimed to determine the role of miR-93 in AMD using a laser-induced CNV mouse model. CNV was induced by laser photocoagulation in C57BL/6 mice. The CNV mice were transfected with scrambled miR or miR-93 mimic. The treatment effect was assessed by fundus photography and fluorescein angiography and confirmed by choroidal flatmount. The expression of miR-93 and VEGF-A in ocular tissues was analysed by quantitative polymerase chain reaction (qPCR) and Western blot. The overexpression effects of miR-93 were also proved on human microvascular endothelial cells (HMECs). Significantly decreased expression of miR-93 was observed by qPCR analysis in CNV mice compared to untreated mice (p < 0.05). VEGF-A messenger RNA (mRNA) and protein expression were upregulated with CNV; these changes were ameliorated by restoration of miR-93 (p < 0.05). CNV was reduced after miR-93 transfection. Transfection of miR-93 reduced the proliferation of HMECs (p < 0.01), but no significant changes were observed in 2D capillary-like tube formation (p > 0.05) and migration (p > 0.05) compared with that in the untreated cells. miR-93 has been shown to be a negative modulator of angiogenesis in the eye. All together, these results highlight the therapeutic potential of miR-93 and suggest that it may contribute as a putative therapeutic target for AMD in humans (AU)


No disponible


Assuntos
Humanos , Animais , Camundongos , Degeneração Macular/genética , MicroRNAs/genética , RNA Mensageiro/genética , Transdução de Sinais , Transfecção , Modelos Animais de Doenças , Células Endoteliais , Regulação da Expressão Gênica , Linhagem Celular , Movimento Celular , Fotocoagulação/efeitos adversos , Angiofluoresceinografia
11.
Rev. neurol. (Ed. impr.) ; 62(supl.1): s3-s8, 21 feb., 2016. ilus
Artigo em Espanhol | IBECS | ID: ibc-151020

RESUMO

Los trastornos de neurodesarrollo están asociados a anomalías funcionales del cerebro que se manifiestan de forma temprana en la vida. Clásicamente se asociaban de manera casi exclusiva con la aparición de discapacidad intelectual y retraso en el desarrollo psicomotor. Las causas de estos trastornos se han descrito parcialmente, incluyendo anomalías por causas genéticas (síndrome de Down, X frágil, etc.), por exposición a factores tóxicos durante el embarazo (síndrome alcohólico fetal), infecciones (citomegalovirus, toxoplasmosis, etc.) o por otras alteraciones, entre las que cabe citar la gran inmadurez en el momento del nacimiento (grandes prematuros). Datos epidemiológicos apoyados en un mejor conocimiento de las enfermedades del sistema nervioso central indican que algunos trastornos mentales, que aparecen en la adolescencia o la madurez temprana, están originados también por anomalías del desarrollo cerebral. Esta revisión pretende dar una visión general del desarrollo cerebral. También se analizan algunos de los procesos celulares y moleculares que pueden explicar las similitudes y diferencias en los fenotipos que generan las alteraciones del desarrollo normal. Todo ello con el objetivo de identificar claramente los procesos sensibles a ser modificados con la actuación terapéutica de un programa de atención temprana (AU)


Neurodevelopmental disorders are associated to functional anomalies of the brain that become manifest early on in life. Traditionally, they have been related almost exclusively to the appearance of intellectual disability and delayed psychomotor development. The causes of these disorders have been partially described, and include anomalies due to genetic causes (Down syndrome, fragile X syndrome, etc.), exposure to toxic factors during pregnancy (foetal alcohol syndrome), infections (cytomegalovirus, toxoplasmosis, etc.) or other alterations, including a status of great immaturity at birth (very preterm). Epidemiological data based on a better knowledge of the diseases affecting the central nervous system suggest that some mental disorders, which appear in adolescence or early adulthood, also have their origin in anomalies in brain development. This review aims to offer an overview of brain development. Some of the cellular and molecular processes that may account for the similarities and differences in the phenotypes that generate alterations affecting normal development are also analysed. The study is conducted with a view to clearly identifying processes that are susceptible to modification by means of therapeutic intervention consisting in an early care programme (AU)


Assuntos
Humanos , Masculino , Feminino , Criança , Adolescente , Cérebro/anormalidades , Cérebro/fisiologia , Córtex Cerebral/crescimento & desenvolvimento , Sistema Nervoso Central/fisiologia , Deficiência Intelectual/etiologia , Deficiências do Desenvolvimento/etiologia , Transtornos Psicomotores/etiologia , Esquizofrenia/etiologia , Transtornos do Neurodesenvolvimento/genética , Transtorno Autístico/etiologia , Desenvolvimento Infantil/fisiologia , Desenvolvimento do Adolescente/fisiologia , Desenvolvimento Embrionário/fisiologia , Neurulação/fisiologia , Disrafismo Espinal , Plasticidade Neuronal/fisiologia , Movimento Celular/fisiologia , Membranas Sinápticas , Exposição Ambiental
12.
Clin. transl. oncol. (Print) ; 17(8): 632-639, ago. 2015. tab, ilus
Artigo em Inglês | IBECS | ID: ibc-138178

RESUMO

Purpose. A novel tumor suppressor gene CKLF-like MARVEL transmembrane domain-containing member 3 (CMTM3) is reduced or undetectable in many kinds of cancers and relates tumor malignant features. We detected its role in prostate cancer for possibility of target therapy as accumulating evidence has shown that CMTM3 is a promising tumor suppressor gene (TSG) for gene therapy. Methods. The expression of CMTM3 detected in prostate tissue microarray, specimens and cell lines were evaluated by immunohistochemistry and semi-quantitative PCR and Western blot, respectively. After being transfected with CMTM3 adenovirus or vector (mock), the proliferation and migration and invasion of LNCaP cells were detected by transwell assay and matrigel assay, respectively. Furthermore, the effects of CMTM3 on tumor growth were performed in nude mice xenograft in vivo. Results. We found CMTM3 was reduced in PCa tissues and cells compared with BPH tissues, and its expression in PCa tissues was related to the Gleason score. Moreover, after being transfected with adenovirus, ectopic expression of CMTM3 in LNCaP cells led to significant inhibition of cell proliferation and migration and invasion compared with the control (P < 0.05), which may be attributed to decreased Erk1/2 activity as p-Erk1/2 was remarkably reduced when CMTM3 was overexpressed. Finally, restoration of CMTM3 significantly suppressed xenograft tumor growth in vivo (P < 0.01) (AU)


No disponible


Assuntos
Animais , Masculino , Camundongos , Genes Supressores de Tumor/fisiologia , Neoplasias da Próstata/diagnóstico , Neoplasias da Próstata/terapia , Neoplasias da Próstata/veterinária , Proteínas com Domínio MARVEL/uso terapêutico , Terapia Genética , Movimento Celular/fisiologia , Proliferação de Células/fisiologia , Ensaios Antitumorais Modelo de Xenoenxerto , Reação em Cadeia da Polimerase , Reação em Cadeia da Polimerase/veterinária , Western Blotting , Western Blotting/veterinária , Imuno-Histoquímica , Terapia Genética/veterinária , Ensaios Antitumorais Modelo de Xenoenxerto/veterinária
13.
Clin. transl. oncol. (Print) ; 17(6): 447-485, jun. 2015. ilus, graf
Artigo em Inglês | IBECS | ID: ibc-138717

RESUMO

Purpose: The present study aimed at investigating the role and potential mechanism of geranylgeranyltransferase I (GGTase-I) on glioma cell migration and invasion. Methods Wound-healing assay and transwell assay were performed to study whether GGTase-I and Ras-like GTPase B (RalB) have effect on glioma cell migration and invasion. Results: We found that knockdown of GGTase-I or RalB both significantly decreased the migratory and invasive abilities of glioma cells. GGTase-I down-regulation suppressed RalB membrane association. Moreover, downregulation of RalB partially abolished the effect of GGTb over-expression-induced glioma cell migration and invasion increase. Conclusions: These findings suggest that RalB might be one of the targets for facilitating the invasive phenotype of malignant gliomas induced by GGTase-I (AU)


No disponible


Assuntos
Humanos , Glioma/patologia , Geranil-Geranildifosfato Geranil-Geraniltransferase/farmacocinética , Proteínas Monoméricas de Ligação ao GTP/farmacocinética , Movimento Celular , Invasividade Neoplásica/patologia
14.
Rev. esp. enferm. dig ; 107(2): 63-71, feb. 2015. ilus
Artigo em Inglês | IBECS | ID: ibc-133092

RESUMO

Background and aims: Statins are reported to have a beneficial effect on portal hypertension (PTH); however, the exact mechanism remains unknown. Hepatic stellate cells (HSCs) can be activated by transforming growth factor beta (TGFβ) and play an important role in angiogenesis leading to PTH. Statins potently stimulate the transcription factor, Kruppel-like factor 2 (KLF2), which can negatively regulate angiogenesis. Our present study aimed to investigate the anti-angiogenic potential of statins in HSCs through the KLF2 pathway. Method: TGFβ-induced human HSCs were exposed to simvastatin. Cell viability and proliferation were determined by MTT and BrdU-proliferation assays, respectively. Cell migration was investigated using a transwell and wound-healing assays. Gene quantification was measured by real-time polymerase chain reaction. Protein expression was detected by western blot analysis and immunohistochemistry. Inflammatory factors were measured using enzyme-linked immunosorbent assays. Result: Simvastatin was found to reduced cell migration and proliferation and inhibit expression of alpha smooth muscle actin in TGFβ-induced HSCs. Furthermore, simvastatin promoted already increased mRNA and protein levels of KLF2 in TGFβ-induced HSCs. In accordance with KLF2 overexpression, simvastatin increased production of endothelial nitric oxide synthesis (eNOS) and downregulated expression of some proangiogenic proteins, such as vascular endothelial growth factor, hypoxia inducible factor-1a and nuclear factor-kappa B in TGFβ-induced HSCs. At the same time, secretion of interferon-gamma increased in TGFβ induced HSCs, which was decreased by simultaneous addition of simvastatin. Conclusion: Simvastatin suppressed the proangiogenic environment of HSCs activated by TGFβ, and KLF2 pathway is involved in the course (AU)


No disponible


Assuntos
Sinvastatina , Fatores de Transcrição Kruppel-Like/uso terapêutico , Inibidores da Angiogênese/uso terapêutico , Células Estreladas do Fígado , Movimento Celular , Sinvastatina/metabolismo , Sinvastatina/farmacocinética , Ensaio de Imunoadsorção Enzimática/métodos , Western Blotting/métodos , Desenvolvimento Experimental
15.
Rev. neurol. (Ed. impr.) ; 57(supl.1): s37-s45, 6 sept., 2013. ilus
Artigo em Espanhol | IBECS | ID: ibc-149004

RESUMO

Las malformaciones congénitas del sistema nervioso central se relacionan con alteraciones en la formación del tubo neural, en las que se incluyen la mayoría de las entidades de tratamiento neuroquirúrgico, disrafismos y craneosinostosis, alteraciones de la proliferación neuronal, microcefalias y megalencefalias, anomalías de la migración neuronal, lisencefalia, paquigiria, esquisencefalia, agenesia del cuerpo calloso, heterotopías y displasias corticales, malformaciones raquimedulares y disrafias medulares. En el presente trabajo se clasifican las diferentes malformaciones del sistema nervioso central susceptibles de corregirse mediante cirugía en el menor tiempo posible y se exponen los mecanismos de génesis de estas lesiones cada vez mejor estudiadas desde las áreas neurogenética y neuroembriológica. Esto involucra la posible conexión de áreas de conocimiento novedosas, como los mecanismos de alteración de la inducción dorsal (cierre del tubo neural) y ventral (telencefalización) con los mecanismos actuales de corrección, y también las anomalías de la proliferación y diferenciación celular de la migración neuronal y, finalmente, el complejo de malformaciones que afectan la fosa posterior y las posibilidades actuales de corrección de éstas (AU)


Congenital malformations of the central nervous system are related to alterations in neural tube formation, including most of the neurosurgical management entities, dysraphism and craniosynostosis; alterations of neuronal proliferation; megalencefaly and microcephaly; abnormal neuronal migration, lissencephaly, pachygyria, schizencephaly, agenesis of the corpus callosum, heterotopia and cortical dysplasia, spinal malformations and spinal dysraphism. We expose the classification of different central nervous system malformations that can be corrected by surgery in the shortest possible time and involving genesis mechanisms of these injuries getting better studied from neurogenic and neuroembryological fields, this involves connecting innovative knowledge areas where alteration mechanisms in dorsal induction (neural tube) and ventral induction (telencephalization) with the current way of correction, as well as the anomalies of cell proliferation and differentiation of neuronal migration and finally the complex malformations affecting the posterior fossa and current possibilities of correcting them (AU)


Assuntos
Humanos , Sistema Nervoso Central/anormalidades , Sistema Nervoso Central/cirurgia , Sistema Nervoso Central/embriologia , Procedimentos Neurocirúrgicos , Malformações do Sistema Nervoso/classificação , Malformações do Sistema Nervoso/cirurgia , Malformações do Sistema Nervoso/embriologia , Síndrome de Dandy-Walker/cirurgia , Doenças Cerebelares/cirurgia , Síndrome de Budd-Chiari/cirurgia , Hidrocefalia , Crânio/cirurgia , Diferenciação Celular , Linhagem da Célula , Movimento Celular , Retina/anormalidades , Retina/cirurgia , Morfogênese , Cerebelo/anormalidades , Anormalidades Múltiplas , Derivação Ventriculoperitoneal , Doenças Renais Císticas/cirurgia , Anormalidades do Olho/cirurgia
16.
Clin. transl. oncol. (Print) ; 15(3): 189-197, mar. 2013. tab, ilus
Artigo em Inglês | IBECS | ID: ibc-127077

RESUMO

INTRODUCTION: Radiation resistance is a major cause of death in cancer patients. Cancer cells react during radiotherapy by re-programming specific cell functions that may confer resistance to radiation. The understanding of this complex process is hindered due to the lack of appropriate study models. We describe an experimental development of a radioresistant isogenic cancer cell line, and its molecular characterization. MATERIALS AND METHODS: A431-cultured cells were irradiated for 7 month until 85 Gy. Then, a selected single cell was left to grow as stable A431-R cell line. Clonogenic assay was used to determine cell survival, the α and β parameters of the LQ model, and the mean inactivation dose. The DNA repair ability of cells was evaluated by pulsed-field electrophoresis method. Differential effect of fractionated radiation was ultimately tested in xenografts. Furthermore, we used a wound healing assay, Western blot for EGFR, AKT and ERK1/2 and ELISA test for vascular endothelial growth factor (VEGF) secretion. Finally we explored CD44 marker and cell cycle distribution. RESULTS: The established A431-R cell line showed radiation resistance in clonogenic assays, repair of radiation-induced DNA fragmentation and xenografted tumours. The radiation resistance was associated with in vitro higher cell growth and migration, increased levels of former oncoproteins, and secretion of VEGF. CONCLUSIONS: In this model, the emergence of radiation resistance was associated with the acquisition of biological traits that support more aggressive behaviour of cancer cells. We have generated a model that will be useful for mechanistic studies and development of rational treatments against radiation resistance in cancer (AU)


Assuntos
Humanos , Animais , Feminino , Camundongos , Carcinoma de Células Escamosas/patologia , Tolerância a Radiação , Receptores de Hialuronatos/metabolismo , Apoptose , Western Blotting , Carcinoma de Células Escamosas/metabolismo , Carcinoma de Células Escamosas/radioterapia , Ciclo Celular , Movimento Celular , Proliferação de Células , Relação Dose-Resposta à Radiação , Citometria de Fluxo , Raios gama , Camundongos Nus , Fenótipo , Células Tumorais Cultivadas , Fator A de Crescimento do Endotélio Vascular , Cicatrização , Ensaios Antitumorais Modelo de Xenoenxerto
17.
Clin. transl. oncol. (Print) ; 15(1): 46-54, ene. 2013. tab, ilus
Artigo em Inglês | IBECS | ID: ibc-126967

RESUMO

BACKGROUND: Recent studies suggest that the relationship between cancer stem cells (CSCs) and the vascular niche may be bidirectional; the niche can support the growth and renewal of CSCs, and CSCs may contribute to the maintenance of the niche. There is little knowledge concerning the role of breast cancer stem cells in promoting tumor angiogenesis. AIM: For human breast cancers, CSCs have been shown to be associated with a CD44+/CD24- phenotype. We investigated the potential activities of CD44+/CD24- breast cancer stem cells in promoting tumor angiogenesis. METHODS: The expression of pro-angiogenic genes was determined by quantitative real-time RT-PCR. Endothelial cell migration assays were employed to evaluate effects of conditioned media from CD44+/CD24- on human umbilical vein endothelial cells. A chorioallantoic membrane (CAM) assay was used to study the potential of CD44+/CD24- cells to promote angiogenesis. RESULTS: In our study, CD44+/CD24- cells expressed elevated levels of pro-angiogenic factors compared with CD44+/CD24+ cells. CD44+/CD24- cell-conditioned media significantly increased endothelial cell migration. Breast cancer cell lines enriched with CD44+/CD24- cells were more pro-angiogenic in the CAM assay than hose lacking a CD44+/CD24- subpopulation. CD44+/CD24- cells sorted from MCF-7 cell lines were more pro-angiogenic in a CAM assay than CD44+/CD24+ cells. Furthermore, the VEGF concentration was significantly higher in CD44+/CD24- cell-conditioned media than in CD44+/CD24+ cell-conditioned media. The pro-angiogenic effect of CD44+/CD24- cells on endothelial cells was abolished by bevacizumab. CONCLUSION: Our findings demonstrate that CD44+/CD24- breast cancer stem cells have substantial pro-angiogenic potential and activity. This provides new insights to explore in the development of targeted therapies (AU)


Assuntos
Humanos , Animais , Feminino , Inibidores da Angiogênese/farmacologia , Anticorpos Monoclonais Humanizados/farmacologia , Neoplasias da Mama/metabolismo , Neoplasias da Mama/patologia , Antígeno CD24/metabolismo , Receptores de Hialuronatos/metabolismo , Linhagem Celular Tumoral , Movimento Celular , Embrião de Galinha , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Membrana Corioalantoide/irrigação sanguínea , Membrana Corioalantoide/metabolismo , Células Endoteliais , Células Endoteliais/fisiologia , Células-Tronco Neoplásicas , Células-Tronco Neoplásicas/metabolismo , Células-Tronco Neoplásicas/patologia , Neovascularização Patológica/metabolismo , Neovascularização Patológica/patologia
18.
Rev. esp. cardiol. (Ed. impr.) ; 62(5): 552-562, mayo 2009. ilus
Artigo em Espanhol | IBECS | ID: ibc-72667

RESUMO

El proceso de extravasación leucocitaria, un paso crucial de la respuesta inflamatoria, implica la migración de los leucocitos desde la corriente sanguínea hasta los tejidos diana donde ejercen su función efectora. La extravasación de los leucocitos está orquestada por la acción conjunta de receptores de adhesión celular y factores quimiotácticos, e implica cambios morfológicos drásticos tanto en leucocitos como en células endoteliales. De este modo, constituye un proceso activo para ambos tipos celulares que promueve la rápida y eficiente llegada de los leucocitos a los focos inflamatorios sin comprometer la integridad de la barrera endotelial. Este artículo revisa la extravasación leucocitaria, con especial hincapié en los hallazgos más recientes en este campo, tanto desde el punto de vista molecular como mecanístico. Incluye la descripción de nuevos pasos en la cascada de adhesión tales como el enlentecimiento del rodamiento, la locomoción intraluminal o la ruta alternativa de migración transcelular, así como el papel funcional de nuevos receptores de adhesión, la organización espaciotemporal de los receptores en la membrana plasmática y las rutas de señalización que controlan los diferentes estadios del proceso de extravasación (AU)


The process of leukocyte extravasation, a critical step in the inflammatory response, involves the migration of leukocytes from the bloodstream towards target tissues, where they exert their effector function. Leukocyte extravasation is orchestrated by the combined action of cellular adhesion receptors and chemotactic factors, and involves radical morphological changes in both leukocytes and endothelial cells. Thus, it constitutes an active process for both cell types and promotes the rapid and efficient influx of leukocytes to inflammatory foci without compromising the integrity of the endothelial barrier. This article provides a review of leukocyte extravasation from both molecular and mechanical points of view, with a particular emphasis on the most recent findings on the topic. It includes a description of newly revealed steps in the adhesion cascade, such as slow rolling motion, intraluminal crawling and alternative pathways for transcellular migration, and discusses the functional role of novel adhesion receptors, the spatiotemporal organization of receptors at the plasma membrane, and the signaling pathways that control different phases of the extravasation process. for transcellular migration, and discusses the functional role of novel adhesion receptors, the spatiotemporal organization of receptors at the plasma membrane and the signaling pathways that control different phases of the extravasation process (AU)


Assuntos
Humanos , Masculino , Feminino , Anti-Inflamatórios/uso terapêutico , Movimento Celular/fisiologia , Endotélio Vascular/fisiologia , Inflamação/patologia , Leucócitos/fisiologia , Anti-Inflamatórios/farmacologia , Adesão Celular , Movimento Celular , Inflamação/tratamento farmacológico , Integrinas/fisiologia , Selectinas/fisiologia
20.
Inmunología (1987) ; 27(4): 192-204, oct.-dic. 2008.
Artigo em Inglês | IBECS | ID: ibc-108109

RESUMO

Los linfocitos T y B migran continuamente desde la sangre hacia los órganos linfoides secundarios, en los cuales antígenos procedentes de tejidos periféricos son procesados y presentados por células presentadoras. Tras permanecer en estos órganos temporalmente, de no producirse el reconocimiento antigénico, los linfocitos abandonan los mismos y son devueltos a la sangre para reiniciar este patrón migratorio conocido como recirculación linfocitaria. El continuo movimiento de los linfocitos a través de estos órganos incrementa la probabilidad de que se produzca el encuentro linfocito-antígeno específico, y es por tanto imprescindible para el eficaz desarrollo de respuestas inmunitarias adaptativas. Los principales factores reguladores del tráfico linfocitario son proteínas de la familia de las quimiocinas y el lípido esfingosina-1-fosfato. Mediante la activación de receptores de membrana, estos mediadores promueven la adhesión de los linfocitos circulantes en el interior de vasos sanguíneos específicos, el acceso a los órganos linfoides, la migración en su interior, y la posterior salida a los conductos linfáticos o la sangre. El objetivo de esta revisión es repasar el estado actual del conocimiento de los mecanismos de señalización intracelular que son activados por estos receptores y que sustentan la continua recirculación linfocitar (AU)


Lymphocytes migrate from the blood stream into secondary lymphoid organs (SLO), where antigens (Ag) collected in the periphery are displayed on the surface of Ag-presenting cells. Continuous lymphocyte recirculation throughout SLO greatly increases the chances that rare Agspecific T and B cells encounter their cognate Ag, making it a prerequisite for effective immune surveillance. Members of the chemokine family of proteins, as well as the lipid mediator sphingosine-1-phosphate (S1P),are the main factors orchestrating dynamic trafficking of lymphocytes. They exert this control by activating specific receptors, which promotelymphocyte adhesion inside specific microvessels of SLO, subsequent migration inside lymphoid tissue and egress into the blood. This article covers our current understanding of the complex intracellular signaling mechanisms that are activated downstream of these receptors and contribute to lymphocyte recirculation (AU)


Assuntos
Humanos , Peptídeos e Proteínas de Sinalização Intracelular/imunologia , Quimiocinas/imunologia , Linfócitos/imunologia , Movimento Celular/imunologia , Adesão Celular/imunologia
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