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1.
Clín. investig. arterioscler. (Ed. impr.) ; 35(1): 1-11, Ene-Feb. 2023. tab, graf
Artigo em Inglês | IBECS | ID: ibc-215760

RESUMO

Objective: Vascular smooth muscle cells (VSMCs) undergo a phenotypic-switching process during the generation of unstable atheroma plaques. In this investigation, the potential implication of the tumor necrosis factor superfamily (TNFSF) ligands, in the gene expression signature associated with VSMC plasticity was studied. Material and methods: Human aortic (ha)VSMCs were obtained commercially and treated with the cytokine TNFSF14, also called LIGHT, the lymphotoxin alpha (LTα), the heterotrimer LTα1β2 or with vehicle for 72h. The effect of the different treatments on gene expression was analyzed by quantitative PCR and included the study of genes associated with myofibroblast-like cell function, osteochondrogenesis, pluripotency, lymphorganogenesis and macrophage-like cell function. Results: HaVSMCs displayed a change in myofibroblast-like cell genes which consisted in reduced COL1A1 and TGFB1 mRNA levels when treated with LTα or LIGHT and with augmented MMP9 expression levels when treated with LTα. LTα and LIGHT treatments also diminished the expression of genes associated with osteochondrogenesis and pluripotency SOX9, CKIT, and KLF4. By contrary, all the above genes were no affected by the treatment with the trimer LTα1β2. In addition, haVSMC treatment with LTα, LTα1β2 and LIGHT altered lymphorganogenic cytokine gene expression which consisted of augmented CCL20 and CCL21 mRNA levels by LTα and a reduction in the gene expression of CCL21 and CXCL13 by LIGHT and LTα1β2 respectively. Neither, LTα or LIGHT or LTα1β2 treatments affected the expression of macrophage-like cell markers in haVSMC. Conclusions: Altogether, indicates that the TNFSF ligands through their interconnected network of signaling, are important in the preservation of VSMC identity against the acquisition of a genetic expression signature compatible with functional cellular plasticity.(AU)


Objetivo: La transición de placa de ateroma estable a placa inestable implica, entre otros procesos, un cambio fenotípico de las células del músculo liso vascular (CMLVs). En esta investigación, se estudió el posible papel de los ligandos de la superfamilia del factor de necrosis tumoral (TNFSF), en los cambios de expresión génica asociada a la plasticidad de las CMLVs. Materiales y métodos: Las CMLVs de aorta humana (CMLVah) se obtuvieron comercialmente y se trataron con la citoquina TNFSF14, también llamada LIGHT, la linfotoxina alfa (LTα), el heterotrímero LTα1β2 o con vehículo durante 72 horas. El efecto de los diferentes tratamientos se analizó mediante el estudio de la expresión génica por PCR cuantitativa e incluyó genes asociados con fenotipo miofibroblástico, osteocondrogénico, genes de pluripotencia, genes de linforganogénesis y genes característicos de macrófagos. Resultados: El estudio de genes asociados a fenotipo miofibroblástico en las CMLVah reveló una reducción de la expresión génica de COL1A1 y TGFB1 tras el tratamiento con LTα o LIGHT mientras que el tratamiento con LTα aumentó los niveles de mRNA de MMP9. LTα y LIGHT también disminuyeron la expresión de genes de osteocondrogénesis y pluripotencia como SOX9, CKIT y KLF4. Por el contrario, la expresión de los genes anteriores no se vio afectada por el tratamiento con el trímero LTα1β2. El tratamiento de las CMLVah con LTα, LTα1β2 y LIGHT alteró la expresión génica de citoquinas linforganogénicas con una expresión aumentada de los genes CCL20 y CCL21 por LTα y una reducción de los niveles de mRNA de CCL21 y CXCL13 por LIGHT y LTα1β2, respectivamente. Ninguno de los tres tratamientos alteró la expresión de genes típicos de macrófagos en las CMLVah. Conclusiones: La presente investigación indica que los ligandos de la familia de los TNFSF a través de su red de señalización...(AU)


Assuntos
Humanos , Células Musculares , Inflamação , Linfotoxina-beta , Plasticidade Celular , Músculo Liso Vascular , Arteriosclerose , Pesquisa
2.
Clín. investig. arterioscler. (Ed. impr.) ; 35(1): 42-51, Ene-Feb. 2023. ilus, tab
Artigo em Inglês | IBECS | ID: ibc-215765

RESUMO

Vascular smooth muscle cells (VSMCs) constitute the principal cellular component of the medial layer of arteries and are responsible for vessel contraction and relaxation in response to blood flow. Alterations in VSMCs can hinder vascular system function, leading to vascular stiffness, calcification and atherosclerosis, which in turn may result in life-threatening complications. Pathological changes in VSMCs typically correlate with chronological age; however, there are certain conditions and diseases, such as Hutchinson-Gilford progeria syndrome (HGPS), that can accelerate this process, resulting in premature vascular aging. HGPS is a rare genetic disorder characterized by severe VSMC loss, accelerated atherosclerosis and death from myocardial infarction or stroke during the adolescence. Because experiments with mouse models have demonstrated that alterations in VSMCs are responsible for early atherosclerosis in HGPS, studies on this disease can provide insights into the mechanisms of vascular aging and assess the relative contribution of VSMCs to this process.(AU)


Las células del músculo liso vascular (CMLV) constituyen el principal componente celular de la capa medial arterial, siendo responsables de la contracción y relajación de los vasos en respuesta al flujo sanguíneo. Las alteraciones en CMLV dificultan la función vascular, generan rigidez vascular, calcificación y aterosclerosis, pudiendo resultar en complicaciones mortales. Cambios patológicos en CMLV suelen correlacionarse con la edad cronológica; sin embargo, existen afecciones y enfermedades, como el síndrome de progeria de Hutchinson-Gilford (HGPS), que pueden acelerar este proceso, provocando envejecimiento vascular prematuro. El HGPS es un trastorno genético raro caracterizado por una pérdida grave de CMLV, aterosclerosis acelerada y muerte por infarto de miocardio o ictus durante la adolescencia. Experimentos con modelos de ratón demostraron que las alteraciones en CMLV son responsables de la aterosclerosis temprana en HGPS. Por tanto, estudios sobre esta enfermedad pueden proporcionar información sobre los mecanismos del envejecimiento vascular y caracterizar la contribución de las CMLV.(AU)


Assuntos
Humanos , Envelhecimento , Aterosclerose , Doenças Cardiovasculares , Músculo Liso Vascular , Progéria , Arteriosclerose , Saúde do Idoso
3.
J. physiol. biochem ; 78(1): 245-256, feb. 2022.
Artigo em Inglês | IBECS | ID: ibc-215886

RESUMO

Abdominal aortic aneurysm (AAA) is a potentially fatal vascular disease, and the dysregulated circular RNAs (circRNAs) play key roles in AAA progression. Circ_0092291 was downregulated in AAA patients, but its function in AAA remains unclear. This research was performed for the functional analysis of circ_0092291 and its mechanism exploration with mircoRNA-626 (miR-626) and collagen type IV alpha1 chain (COL4A1) in AAA. Human aortic vascular smooth muscle cells (T/G HA-VSMC) were treated with angiotensin II (Ang II). Levels of circ_0092291, miR-626, and COL4A1 were determined using reverse transcription–quantitative polymerase chain reaction (RT-qPCR). Inflammatory cytokines were examined by enzyme-linked immunosorbent assay (ELISA). Cell apoptosis was measured using caspase3 activity assay and flow cytometry. Angiopoiesis was assessed via tube formation assay. The protein analysis was conducted by western blot. Dual-luciferase reporter assay, RNA immunoprecipitation (RIP), and RNA pull-down assays were used to validate the molecular binding. Circ_0092291 downregulation was found in AAA samples and Ang II-treated cells. Inflammatory response and cell apoptosis were reduced while angiopoiesis and ECM level were facilitated after overexpression of circ_0092291 in Ang II-treated T/G HA-VSMC cells. MiR-626 was a miRNA target for circ_0092291, and miR-626 inhibition protected T/G HA-VSMC from Ang II–induced cell injury. Moreover, the regulation of circ_0092291 was achieved by serving as a miR-626 sponge in Ang II-treated cells. COL4A1 was affirmed as a target for miR-626 and circ_0092291 resulted in the level change of COL4A1 by sponging miR-626. Additionally, miR-626 downregulation inhibited the cell damages caused by Ang II through increasing the level of COL4A1 and the function of circ_0092291 was attributed to the upregulation of COL4A1. (AU)


Assuntos
Humanos , Angiotensina II/metabolismo , MicroRNAs/genética , MicroRNAs/metabolismo , Músculo Liso Vascular/metabolismo , Miócitos de Músculo Liso/metabolismo , Colágeno Tipo IV/metabolismo , RNA
4.
J. physiol. biochem ; 74(1): 17-24, feb. 2018. tab, graf, ilus
Artigo em Inglês | IBECS | ID: ibc-178914

RESUMO

The number of patients with adrenal aldosterone-producing adenomas (APAs) has gradually increased. However, even after adenoma resection, some patients still suffer from high systolic blood pressure (SBP), which is possibly due to great arterial remodeling. Moreover, mineralocorticoid receptors (MRs) were found to be expressed in vascular smooth muscle cells (VSMCs). This study aims to determine whether MR antagonism protects the aorta from aldosterone-induced aortic remolding. Male rats were subcutaneously implanted with an osmotic minipumps and randomly divided into four groups: control; aldosterone (1 μg/h); aldosterone plus a specific MR antagonist, eplerenone (100 mg/kg/day); and aldosterone plus a vasodilator, hydralazine (25 mg/kg/day). After 8 weeks of infusion, aortic smooth muscle cell proliferation and collagen deposition, as well as the MDM2 and TGF-Beta1 expression levels in the aorta, were examined. Model rats with APAs were successfully constructed. Compared with the control rats, the model rats exhibited (1) marked SBP elevation, (2) no significant alteration in aortic morphology, (3) increased VSMC proliferation and MDM2 expression in the aorta, and (4) enhanced total collagen and collagen III depositions in the aorta, accompanied with up-regulated expression of TGF- Beta1. These effects were significantly inhibited by co-administration with eplerenone but not with hydralazine. These findings suggested that specific MR antagonism protects the aorta from aldosterone-induced VSMC proliferation and collagen deposition


Assuntos
Animais , Masculino , Corticotrofos , Colágeno/metabolismo , Modelos Animais de Doenças , Hipertensão/prevenção & controle , Antagonistas de Receptores de Mineralocorticoides/uso terapêutico , Espironolactona/análogos & derivados , Anti-Hipertensivos/uso terapêutico , Proliferação de Células , Hipertensão/etiologia , Músculo Liso Vascular/metabolismo , Músculo Liso Vascular/patologia , Espironolactona/uso terapêutico , Vasodilatadores/uso terapêutico , Remodelação Vascular
5.
Rev. osteoporos. metab. miner. (Internet) ; 9(4): 130-138, nov.-dic. 2017. graf, ilus, tab
Artigo em Espanhol | IBECS | ID: ibc-169413

RESUMO

Introducción: El calcitriol, fundamental para mantener la homeostasis del calcio y el fósforo en el organismo, puede perjudicar al sistema vascular a dosis elevadas, aumentando el riesgo de calcificación. Objetivo: Evaluar la expresión diferencial de proteínas en células de músculo liso vascular sometidas a una dosis suprafisiológica de calcitriol. Material y métodos: Se cultivaron células de músculo liso vascular de rata (SMAC-R) en presencia de 10-7 M de calcitriol durante 10 días. Se valoró el cambio de fenotipo muscular a óseo mediante actividad fosfatasa alcalina, inmunocitoquímica, reacción en cadena de la polimerasa cuantitativa a tiempo real (qPCR) y Western blot. Mediante electroforesis bidimensional y espectrometría de masas se evaluó el patrón diferencial de proteínas en presencia y ausencia de 10-7 M de calcitriol. Resultados: La exposición a una dosis alta de calcitriol disminuyó significativamente la expresión génica de elastina y la expresión génica y proteica de α-actina, aumentado la expresión génica de osteocalcina y Runx2 y la proteica de osteoprotegerina. A nivel proteómico se identificaron 10 proteínas diferencialmente expresadas, destacando el aumento en superóxido dismutasa mitocondrial, proteínas del citoesqueleto, de formación de vesículas y del inflamasoma. Por el contrario, hubo 4 proteínas que disminuyeron su expresión, destacando alguna de tipo muscular. Conclusiones: En un modelo de células de músculo liso vascular sometidas a una dosis suprafisiológica de calcitriol se observó un aumento de expresión de proteínas del citoesqueleto, que forman vesículas de matriz y que participan en depurar radicales libres y en la respuesta inflamatoria. La pérdida de fenotipo muscular se vio representada por descensos en la expresión de proteínas típicamente musculares (AU)


Introduction: Calcitriol, essential for maintaining calcium and phosphorus homeostasis in the body, may damage the vascular system in high doses, increasing the risk of calcification. Objective: To assess the differential expression of proteins in vascular smooth muscle cells subjected to a supra-physiological dose of calcitriol. Material and methods: Rat vascular smooth muscle cells (VSMC-R) were cultured in the presence of 10-7 M calcitriol for 10 days. The change of muscle to bone phenotype was assessed by alkaline phosphatase activity, immunocytochemistry, quantitative polymerase chain reaction in time (QPCR) and Western blot analysis. By means of two-dimensional electrophoresis and mass spectrometry was evaluated for the differential protein pattern in presence and absence of 10-7 M calcitriol. Results: Exposure to a high dose of calcitriol decreased elastin gene expression and the protein and gene expression of α-actin protein, increased gene expression of osteocalcin and Runx2 and expression of osteoprotegerin protein. At the proteomic level, 10 differentially expressed proteins were identified, highlighting the increase in mitochondrial superoxide dismutase, cytoskeleton proteins, vesicle formation and inflammasome. On the contrary, there were 4 proteins that diminished expression, highlighting some of muscular type. Conclusions: In a model of vascular smooth muscle cells submitted to a supra-physiological dose of calcitriol an increased expression of cytoskeleton proteins was observed. These proteins form matrix vesicles and participate in clearance of free radicals and in the inflammatory response. The loss of muscle phenotype was represented by decreased expression of typically muscle proteins (AU)


Assuntos
Humanos , Relação Dose-Resposta a Droga , Calcitriol/metabolismo , Calcitriol/uso terapêutico , Músculo Liso Vascular , Músculo Liso Vascular/metabolismo , Miócitos de Músculo Liso , Músculo Liso Vascular/citologia , Calcinose/tratamento farmacológico , Calcificação Vascular/tratamento farmacológico , Proteômica/métodos , Proteômica/normas
6.
Clín. investig. arterioscler. (Ed. impr.) ; 28(4): 167-177, ago. 2016. ilus, graf, tab
Artigo em Inglês | IBECS | ID: ibc-155197

RESUMO

Introduction: microRNA (miRNA) expression profile of extracellular vesicles is a potential tool for clinical practice. Despite the key role of vascular smooth muscle cells (VSMC) in cardiovascular pathology, there is limited information about the presence of miRNAs in microparticles secreted by this cell type, including human coronary artery smooth muscle cells (HCASMC). Here, we tested whether HCASMC-derived microparticles contain miRNAs and the value of these miRNAs as biomarkers. Methods: HCASMC and explants from atherosclerotic or non-atherosclerotic areas were obtained from coronary arteries of patients undergoing heart transplant. Plasma samples were collected from: normocholesterolemic controls (N=12) and familial hypercholesterolemia (FH) patients (N=12). Both groups were strictly matched for age, sex and cardiovascular risk factors. Microparticle (0.1-1μm) isolation and characterization was performed using standard techniques. VSMC-enriched miRNAs expression (miR-21-5p, -143-3p, -145-5p, -221-3p and -222-3p) was analyzed using RT-qPCR. Results: Total RNA isolated from HCASMC-derived microparticles contained small RNAs, including VSMC-enriched miRNAs. Exposition of HCASMC to pathophysiological conditions, such as hypercholesterolemia, induced a decrease in the expression level of miR-143-3p and miR-222-3p in microparticles, not in cells. Expression levels of miR-222-3p were lower in circulating microparticles from FH patients compared to normocholesterolemic controls. Microparticles derived from atherosclerotic plaque areas showed a decreased level of miR-143-3p and miR-222-3p compared to non-atherosclerotic areas. Conclusions: We demonstrated for the first time that microparticles secreted by HCASMC contain microRNAs. Hypercholesterolemia alters the microRNA profile of HCASMC-derived microparticles. The miRNA signature of HCASMC-derived microparticles is a source of cardiovascular biomarkers


Introducción: Los datos sobre la presencia de microARN en micropartículas liberadas por células de músculo liso vascular (VSMC) y en particular de las células de músculo liso de arteria coronaria humana (HCASMC) son limitados. Por ello, hemos analizado el contenido de miARN en micropartículas liberadas por HCASMC y su posible potencial como biomarcadores. Métodos: Los explantes de arterias coronarias se obtuvieron de pacientes sometidos a trasplante de corazón. Las muestras de plasma se obtuvieron de 2 grupos de estudio: controles normocolesterolémicos (n=12) y pacientes con hipercolesterolemia familiar (HF) (n=12). El aislamiento de micropartículas (0,1-1μm) se llevó a cabo mediante técnicas estándar. La expresión de los miARN típicos de VSMC (miR-21-5p, -143-3p, -145-5p, -221-3p y -222-3p) se analizó mediante RT-qPCR. Resultados: El ARN total aislado a partir de micropartículas procedentes de HCASMC presentó miARN típicos de VSMC. La exposición de HCASMC a condiciones de hipercolesterolemia indujo la reducción en la expresión de miR-143-3p y de miR-222-3p en las micropartículas. Los niveles de expresión de miR-222-3p en micropartículas circulantes fueron inferiores en pacientes de HF en comparación con controles normocolesterolémicos. Las micropartículas liberadas por áreas de placa aterosclerótica mostraron una disminución de los niveles de miR-143-3p y de miR-222-3p en comparación con las de áreas no ateroscleróticas. Conclusiones: Demostramos la presencia de microARN en micropartículas liberadas por HCASMC. La exposición celular a hipercolesterolemia altera el perfil de microARN de estas micropartículas. El perfil de microARN de micropartículas liberadas por HCASMC es una fuente de biomarcadores


Assuntos
Humanos , MicroRNAs/análise , Micropartículas Derivadas de Células/fisiologia , Doença das Coronárias/fisiopatologia , Doença da Artéria Coronariana/fisiopatologia , Biomarcadores/análise , Músculo Liso Vascular/fisiopatologia , Doenças Cardiovasculares/fisiopatologia
7.
J. physiol. biochem ; 72(2): 245-253, jun. 2016. graf
Artigo em Inglês | IBECS | ID: ibc-168269

RESUMO

We previously observed that sarcoendoplasmic reticulum Ca2+ ATPase (SERCA) blockade by cyclopiazonic acid (CPA) significantly potentiates serotonin (5-hydroxytryptamine (5-HT))-induced vascular contractions. Furthermore, 5-HT receptor antagonist methysergide partially inhibited CPA-potentiated 5-HT contractions. In the present study, we further investigated whether SERCA inhibition potentiates 5-HT-induced Ca2+ responses along with attenuating the receptor antagonism by store-operated Ca2+ (SOC) entry and protein kinase C (PKC)-mediated mechanisms. The effects of dexamethasone that was previously shown to induce SOC entry and enhance 5-HT responses were also tested. For this purpose, intracellular Ca2+ levels were monitored in A7r5 embryonic rat vascular smooth muscle cells by spectrofluorometry using the fluorescent indicator fura-2. The results showed that CPA, although not dexamethasone, significantly potentiated 5-HT-induced Ca2+ elevations. Ketanserin partially decreased 5-HT-induced and CPA-potentiated Ca2+ elevations whereas both PKC inhibitor D-sphingosine and SOC entry blocker 2-aminoethoxydiphenyl borate (2-APB) abolished the remaining responses. The data suggests that diminished antagonistic effect on 5-HT-induced Ca2+ elevations in the presence of SERCA inhibition is induced by SOC entry and PKC activation (AU)


No disponible


Assuntos
Animais , Ratos , Sinalização do Cálcio , Inibidores Enzimáticos/farmacologia , Indóis/farmacologia , Músculo Liso Vascular , Agonistas do Receptor de Serotonina/farmacologia , Serotonina/metabolismo , ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático/antagonistas & inibidores , Anti-Inflamatórios , Bloqueadores dos Canais de Cálcio/farmacologia , Antagonistas da Serotonina/farmacologia , Vasoconstritores , Vasodilatadores , Proteína Quinase C , Linhagem Celular
8.
J. physiol. biochem ; 71(4): 785-793, dic. 2015.
Artigo em Inglês | IBECS | ID: ibc-145730

RESUMO

In traditional herbal medicine, Rock Tea (Jasonia glutinosa) is known for its prophylactic and therapeutic value in various disorders including arterial hypertension. However, the mechanism by which Rock Tea exerts blood pressure-lowering actions has not been elucidated yet. Our aim was to demonstrate vasorelaxing effects of Rock Tea extract and to reveal its possible action mechanism. Isometric myography was conducted on high-K+-precontracted rings from rat thoracic aorta and tested extracts at concentrations of 0.5-5 mg/ml. Whole-cell patch-clamp experiments were performed in rat aortic vascular smooth muscle cells (line A7r5) to determine blocking effects on L-type Ca2+ channels. Rock Tea extract relaxed the aorta contracted by high [K+] concentration dependently with an EC50 of ≈2.4 mg/ml and produced ≈75 % relaxation at the highest concentration tested. The L-type Ca2+ channel blocker, verapamil (10−6 M), had similar effects. Rock Tea extract had no effect in nominally Ca2+-free high-K+ buffer but significantly inhibited contractions to re-addition of Ca2+. Rock Tea extract inhibited the contractions induced by the L-type Ca2+ channel activator Bay K 8644 (10−5 M) and by phenylephrine (10−6 M). Rock Tea extract and Y-27632 (10−6 M), Rho-kinase inhibitor, had similar effects and the respective effects were not additive. Patch-clamp experiments demonstrated that Rock Tea extract (2.5 mg/ml) virtually abolished L-type Ca2+ currents in A7r5. We conclude that Rock Tea extract produced vasorelaxation of rat aorta and that this relaxant effect is mediated by inhibition of L-type Ca2+ channels. Rock Tea extracts may be of phytomedicinal value for prevention and adjuvant treatment of hypertension and other cardiovascular diseases


Assuntos
Animais , Ratos , Aorta , Músculo Liso Vascular , Canais de Cálcio , Chá/química , Extratos Vegetais/farmacocinética , Bloqueadores dos Canais de Cálcio/farmacocinética , Doenças Cardiovasculares/prevenção & controle , Vasodilatação
9.
J. physiol. biochem ; 69(4): 945-955, dic. 2013.
Artigo em Inglês | IBECS | ID: ibc-121652

RESUMO

Abnormally functioning K+ channels during aging might contribute to increased arterial tone of vascular smooth muscle cells. However, changes in large conductance calcium-activated potassium (BKca) channel current density and channel protein composition during aging are not fully understood and are currently investigated here. Spontaneously hypertensive rats (SHR) and Wistar–Kyoto (WKY) rats were grouped by age into very young (4–6 weeks), young (16–18 weeks), and adult (40–42 weeks) rats. BKca current was measured using a whole cell patch clamp in vascular smooth muscle cells from rat mesenteric arteries. BKca channel and subunits were measured using confocal imaging and real-time reverse transcriptase polymerase chain reaction techniques. Systolic and diastolic blood pressure increased significantly with age in both SHR and WKY rats. The expression of BKca á subunits increased in plasma membrane and cytoplasm in both SHR and WKY rats during aging, but had a larger increase in the cytoplasm in SHR than in WKY rats. BKca current density increased with aging in SHR but not in WKY rats. The relative abundance of BKca áand â1 mRNA transcripts changed minimally or not at all with aging in both SHR and WKY rats. In conclusion, plasma membrane BKca protein increased with aging in both SHR and WKY rats. Increases in cytoplasmic BKca protein and in BKca current were greater in SHR than WKY rats (AU)


Assuntos
Animais , Ratos , Músculo Liso Vascular/fisiopatologia , Canais de Cálcio/farmacocinética , Canais de Potássio Cálcio-Ativados/farmacocinética , Modelos Animais de Doenças , Ratos Endogâmicos SHR/fisiologia , Fatores Etários
10.
Clín. investig. arterioscler. (Ed. impr.) ; 24(3): 115-130, mayo-jun. 2012. ilus, tab
Artigo em Espanhol | IBECS | ID: ibc-105085

RESUMO

Introducción La hipoxia se considera un factor clave en la progresión de las lesiones ateroscleróticas. El low density lipoprotein receptor-related protein-1 (LRP1) juega un papel fundamental en la vasculatura. El propósito de este estudio fue investigar el efecto de la hipoxia en la expresión y la función del LRP1 en células musculares lisas vasculares (CMLV) y el papel del factor de transcripción inducible por la hipoxia 1 alfa (..) (AU)


Objective Hypoxia is considered a key factor in the progression of atherosclerotic lesions. Low density lipoprotein receptor-related protein 1 (LRP1) plays a pivotal role in the vasculature. The aims of this study were to investigate the effect of hypoxia on LRP1 expression and function in vascular smooth muscle cells (VSMC) and the role of hypoxia-inducible factor alpha (..) (AU)


Assuntos
Humanos , Hipóxia Celular/fisiologia , Aterosclerose/fisiopatologia , Proteína-1 Relacionada a Receptor de Lipoproteína de Baixa Densidade/fisiologia , Músculo Liso Vascular/fisiologia , Esterol Esterase , Lipoproteínas LDL , Subunidade alfa do Fator 1 Induzível por Hipóxia/fisiologia
12.
J. physiol. biochem ; 67(4): 539-549, dic. 2011.
Artigo em Inglês | IBECS | ID: ibc-122391

RESUMO

No disponible


The alteration and further damage of vascular smooth muscle function have been implicated in the development of vascular complications and diabetes. Little is known about protein tyrosine nitration in vascular smooth muscle cell injury induced by high glucose. In this article, vascular smooth muscle cell was exposed to 30 and 40 mM high glucose for 72 h, and then the cell injury in vascular smooth muscle cell induced by high glucose was studied. It was found that high glucose stimulated vascular smooth muscle cell injury in a dose-dependent manner, including decreasing intracellular and extracellular glutathione contents, increasing malondialdehyde and intracellular reactive oxygen species content, increasing the production of nitric oxide (increased nitrite content in cell and medium), as well as increasing protein tyrosine nitration. By comparing protein tyrosine nitration induced by high glucose conditions and extrinsic factors (hemin–nitrite–glucose oxidase system and 3-morpholinosydnonimine), it may be speculated that protein is nitrated selectively, and specific protein tyrosine nitration is involved in diabetic vascular complications (AU)


Assuntos
Animais , Ratos , Proteínas Tirosina Quinases/fisiologia , Músculo Liso Vascular/fisiologia , Angiopatias Diabéticas/fisiopatologia , Hiperglicemia/fisiopatologia , 51919 , Glucose/farmacocinética
13.
J. physiol. biochem ; 67(4): 589-593, dic. 2011.
Artigo em Inglês | IBECS | ID: ibc-122396

RESUMO

No disponible


Sivelestat sodium hydrate (sivelestat) is a novel synthetic drug and specific inhibitor of neutrophil elastase that has been approved in Japan as a treatment for acute lung injury associated with systemic inflammatory response syndrome. It is important to determine how sivelestat affects hemodynamics and the regulatory mechanisms of vascular smooth muscle (VSM). We recently found that sivelestat relaxes porcine coronary artery VSM via selective inhibition of Ca2+ sensitization induced by a receptor agonist without affecting the normal Ca2+-induced contraction. Although sivelestat relaxes porcine artery, its effects on human artery are unknown; therefore, the purpose of the present study was to assess the effects of sivelestat on human artery. In the present study, sivelestat induced concentration-dependent (1 × 10−6 to 3 × 10−4 M) vasorelaxation in U46619 (1 nM) and sphingosylphosphorylcholine (SPC) (30 mM)-precontracted human gastric artery with or without endothelium, but sivelestat did not induce vasorelaxation in conditions of high K+ (40 mM) depolarization. Sivelestat inhibited VSM contraction by an agonist and SPC, and it did not affect Ca2+-induced normal physiologic contraction (AU)


Assuntos
Humanos , Proteínas Secretadas Inibidoras de Proteinases/farmacocinética , Síndrome de Resposta Inflamatória Sistêmica/tratamento farmacológico , Lesão Pulmonar Aguda/tratamento farmacológico , Músculo Liso Vascular , Contração Muscular
15.
J. physiol. biochem ; 67(1): 35-42, mar. 2011. ilus
Artigo em Inglês | IBECS | ID: ibc-122632

RESUMO

No disponible


Telomeres are specialized DNA–protein complexes found at the tips of linear chromosomes. In this study, we investigated the effects of oxidative stress on telomeric length distribution of proliferating vascular smooth muscle cells following balloon injury in single or combined treatment of rabbits with either buthionine sulfoximine or taurine. Exposure to oxidative stress increased the balloon injury whereas taurine treatment significantly diminished l-buthionine-sulfoximine-related intimal hyperplasia. Our results also showed that both variables had a significant influence on mean telomeric length distribution (AU)


Assuntos
Animais , Coelhos , Estresse Oxidativo/fisiologia , Homeostase do Telômero/fisiologia , Músculo Liso Vascular/fisiologia , Angioplastia com Balão , Taurina/farmacocinética , Butionina Sulfoximina/farmacocinética , Modelos Animais de Doenças , Substâncias Protetoras/farmacocinética
16.
J. physiol. biochem ; 65(2): 105-112, abr.-jun. 2009. tab
Artigo em Inglês | IBECS | ID: ibc-75571

RESUMO

High intensity strength training causes changes in steroid hormone concentrations.This could be altered by the muscular contraction type: eccentric or concentric.The aim of this study was to compare the effect of the completion of a short concentric(CON) and concentric/eccentric (CON/ECC) trial on the urinary steroidprofile, both with the same total work. 18 males performed the trials on an isokineticdynamometer (BIODEX III) exercising quadriceps muscles, right and left, on differentdays. Trial 1(CON): 4x10 Concentric knee extension + relax knee flexion,speed 60º/second; rest 90 seconds between each series and 4 minutes between each legexercise. Trial 2(CON/ECC): 4x5 concentric knee extension + Eccentric knee flexionunder similar conditions. Urine samples were taken before the exercise and onehour after finishing it. Androsterone, Etiocholanolone, DHEA, Androstenedione,Testosterone, Epitestosterone, Dehydrotestosterone, Estrone, B-Estradiol, Tetrahydrocortisone,Tetrahydrocortisol, Cortisone and Cortisol (free, glucoconjugated andsulfoconjugated) urinary values were determined using gas chromatography/massspectrometry techniques. No significant differences were noted in Total Work andAverage Peak Torque, although Maximum Peak Torque in the CON/ECC trial washigher than in the CON trial. These results demonstrate no changes in the steroidprofile before and after trials, or when comparing CON to CON/ECC trials. Thedata suggest that eccentric contractions do not cause hormonal changes different tothe ones produced by concentric contractions, when they are performed in strengthshort trials with the same total workload(AU)


El entrenamiento de fuerza de alta intensidad provoca variaciones en la concentración de esteroides. El tipo de contracción muscular, excéntrica o concéntrica, podría ser un factor que la alterase. El objetivo de este estudio fue comparar el efecto de la realización de una sesión corta de ejercicio concéntrico (CON) y otra concéntrica/excéntrica (CON/EXC), con la misma carga de trabajo total, sobre el perfil esteroideo urinario. 18 hombres realizaron dos sesiones de ejercicio de corta duración utilizando una máquina isocinética (BIODEX III) en días diferentes y trabajando los músculos cuádriceps de ambas piernas. La sesión de ejercicio 1 (CON) fue un 4 x 10 rep de extensión concéntrica de rodilla más relajación en el movimiento de flexión, a una velocidad de 60º/segundo y con una recuperación de 90 seg. entre cada serie y 4 minutos entre cada una de las piernas. La sesión de ejercicio 2 (CON/EXC) fue un 4x 5 rep. de extensión concéntrica de rodilla más flexión excéntrica de rodilla, con las mismas condiciones de velocidad y recuperación. Muestras de orina fueron se tomaron antes del ejercicio y una hora después de finalizarlo. Los niveles urinarios (fracción libre, glucoconjugada y sulfoconjugada) de Androsterona, Etiocolanolona, DHEA, Androstenodiona, Testosterona, Epitestosterona, Dehidrotestosterona, Estrona, β-estradiol, Tetrahidrocortisona, Tetrahidrocortisol, Cortisona y Cortisol, se determinaron usando técnicas de cromatografía de gases espectrometría de masas. No se encontraron diferencias significativas en los valores de Trabajo Total y de Pico Torque Medio, aunque los valores de Pico Torque Máximo fueron más alto en el CON/EXC ejercicio que en el CON(AU)


Tampoco se observó ningún cambio en el perfil esteroideo urinario entre antes y después de las sesiones de ejercicio, o comparando las sesiones CON/EXC con la CON. Por tanto, los datos sugieren que las contracciones excéntricas no producen alteraciones hormonales diferentes a las producidas por las contracciones concéntricas, cuando se trata de sesiones de ejercicio de fuerza de corta duración con similar carga de trabajo total(AU)


Assuntos
Humanos , Masculino , Feminino , Genisteína , Retículo Sarcoplasmático , Músculo Liso Vascular , Isoflavonas , Canais de Cálcio , Canais de Cálcio/uso terapêutico
17.
J. physiol. biochem ; 63(2): 143-152, abr.-jun. 2007. ilus
Artigo em Inglês | IBECS | ID: ibc-76671

RESUMO

The soy-derived isoflavones genistein and daidzein affect the contractile state ofdifferent kinds of smooth muscle. We describe acute effects of genistein and daidzeinon contractile force and intracellular Ca2+ concentration ([Ca2+]i) in in situ smoothmuscle of rat aorta. Serotonin (5-HT) (2 ìM) or a depolarizing high K+ solution producedthe contraction of aortic rings, which were immediately relaxed by 20 ìMgenistein and by 20 ìM daidzein. Accordingly, both 5-HT and a high K+ solutionincreased the [Ca2+]i in in situ smooth muscle cells. Genistein strongly inhibited the[Ca2+]i increase evoked by 5-HT (74.0 ± 7.3%, n=11, p<0.05), and had a smallereffect on high K+ induced [Ca2+]i increase (19.9 ± 4.0%, n=7, p<0.05). The K+ channelsblocker tetraethylammonium (TEA) (0.5 mM) diminished genistein effects on 5-HT-induced [Ca2+]i increase. Interestingly, during prolonged application of 5-HT,the [Ca2+]i oscillated and a short (90 s) preincubation with genistein (20 ìM) significantlydiminished the frequency of the oscillations. This effect was totally abolishedby TEA. In conclusion, in rat aortic smooth muscle, genistein is capable of diminishingthe increase in [Ca2+]i and in force evoked by 5-HT and high K+ solution, andof decreasing the frequency of [Ca2+]i oscillations induced by 5-HT. The short timerequired by genistein, and the relaxing effect of daidzein suggest that tyrosine kinasesinhibition is not involved. The small inhibiting effect of genistein on the [Ca2+]iincrease evoked by high K+ and the effect of TEA point to the activation by genisteinof calcium-activated K+ channels (AU)


No disponible


Assuntos
Animais , Masculino , Ratos , Aorta Torácica/citologia , Cálcio/antagonistas & inibidores , Genisteína/farmacologia , Contração Muscular , Músculo Liso Vascular , Serotonina/farmacologia , Citofotometria/métodos , Contração Isométrica , Oscilometria/métodos , Ratos Wistar
18.
J. physiol. biochem ; 63(2): 161-170, abr.-jun. 2007. ilus, tab, graf
Artigo em Inglês | IBECS | ID: ibc-76673

RESUMO

In order to observe the effects of nicotine on protein expression in rat vascularsmooth muscle cells (SMCs), nicotine treated SMCs were studied by proteomic technologiescombining two-dimensional electrophoresis (2-DE) and peptide mass fingerprinting(PMF). Real-time RT–PCR was used to validate the differentiallyexpressed proteins. We found that 11 protein spots were significantly up-regulatedand one down-regulated by nicotine treatment. The results of PMF showed thatthese up- and down-regulated proteins could be divided into three groups accordingto their functions: cytoskeleton proteins, regulatory proteins and enzymes. Simultaneously,we also verified their consistent alteration at the transcriptional levelthrough real-time RT–PCR. The affected proteins turned out to be mainly associatedwith cell migration, proliferation and energy metabolism, and are responsible fornicotine-related cardiovascular damage (AU)


No disponible


Assuntos
Animais , Masculino , Ratos , Músculo Liso Vascular , Nicotina/farmacologia , Proteínas/metabolismo , Proteoma/análise , Proteômica/métodos , Células Cultivadas , Eletroforese em Gel Bidimensional , Imuno-Histoquímica , Espectrometria de Massas , Mapeamento de Peptídeos , Proteínas/genética , Ratos Wistar , Reprodutibilidade dos Testes , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Transcrição Gênica , Tripsina/farmacologia
19.
Rev. esp. cardiol. (Ed. impr.) ; 60(5): 501-509, mayo 2007. ilus, tab
Artigo em Es | IBECS | ID: ibc-058026

RESUMO

Introducción y objetivos. Las propiedades viscoelásticas y geométricas arteriales determinan la poscarga dinámica ventricular. Factores vasoactivos producidos en la adventicia modulan el tono arterial. Resta por establecer si la adventicia participa en la determinación del valor de poscarga dinámica. El objetivo de este estudio fue caracterizar el papel de la adventicia en la determinación de la poscarga dinámica mediante mecanismos dependientes del músculo liso. Métodos. La presión, el diámetro y el flujo se midieron en troncos braquiocefálicos ovinos antes y después de extraerles la adventicia, en estudios in vivo con reactividad muscular intacta (n = 8) e in vitro con reactividad muscular abolida (n = 8). Las arterias se estudiaron en condiciones hemodinámicas similares. La poscarga dinámica se caracterizó mediante la respuesta elástica y viscosa arterial, el trabajo elástico y viscoso, la impedancia característica arterial y la velocidad de propagación del pulso. Comparar los estudios in vivo e in vitro permitió caracterizar los cambios en la activación dependientes del músculo. Resultados. Sólo in vivo la extracción de la adventicia determinó una reducción del diámetro (desde 17,32 ± 2,02 hasta 15,46 ± 1,28 mm) e incrementos en las respuestas elástica (desde 7,21 ± 1,39 hasta 15,59 ± 3,00 106 dinas · cm-2) y viscosa (desde 5,16 ± 2,04 hasta 9,87 ± 2,00 105 dinas · cm-2), en los trabajos elástico (desde 6,15 ± 1,08 hasta 9,20 ± 0,76 x 10-2 J/m2) y viscoso (desde 11,61 ± 2,25 hasta 15,20 ± 2,37 x 10-3 J/m2), en la impedancia arterial (desde 223,97 ± 136,11 hasta 396,33 ± 182,27 dinas · s · cm-3) y velocidad de propagación (desde 397,70 ± 31,21 hasta 598,78 ± 28,04 cm · s-1) (p < 0,05). El menor diámetro y los aumentos en las respuestas elástica y viscosa evidenciaron la activación muscular. Conclusiones. La adventicia participaría en el control de la poscarga dinámica ventricular mediante mecanismos dependientes del tono muscular (AU)


Introduction and objectives. Ventricular dynamic afterload depends on arterial viscoelastic and geometric properties. Vasoactive factors produced in the adventitia modulate arterial tone. However, it is still not known whether the adventitia is involved in determining the magnitude of the dynamic afterload. The aim of this study was to investigate the role played by the adventitia, via smooth muscle-dependent mechanisms, in determining dynamic afterload. Methods. The diameter, pressure and flow in brachiocephalic trunks from sheep were measured before and after removal of the adventitia, both in vivo with muscular reactivity preserved (n=8) and in vitro with muscular reactivity abolished (n=8). All studies were performed under similar hemodynamic conditions. Dynamic afterload was determined from elastic and viscous arterial responses, elastic and viscous work, arterial characteristic impedance, and pulse wave velocity. Comparison of in vivo and in vitro findings enabled smooth muscle-dependent changes to be evaluated. Results. Only in vivo, did removal of the adventitia lead to a reduction in vessel diameter (17.32 [2.02] vs 15.46 [1.28] mm) and to increases in elastic (7.21 [1.39] vs 15.59 [3.00] x 106 dyn.cm-2) and viscous (5.16 [2.04] vs 9.87 [2.00] x 105 dyn.s.cm-2) arterial responses, elastic (6.15 [1.08] vs 9.20 [0.76] x 10-2 J/m2) and viscous work (11.61 [2.25] vs 15.20 [2.37] x 10-3 J/m2), impedance (223.97 [136.11] vs 396.33 [182.27] dyn · s · cm-3), and pulse wave velocity (397.70 [31.21] vs 598.78 [28.04] cm.s-1) (P<.05). The reduction in diameter and the increases in elastic and viscous responses are evidence of muscular activation. Conclusions. The adventitia may contribute to the control of ventricular dynamic afterload by means of mechanisms dependent on muscular tone (AU)


Assuntos
Humanos , Função Ventricular Esquerda/fisiologia , Músculo Liso Vascular/fisiologia , Impedância Elétrica , Frequência Cardíaca , Hemodinâmica
20.
Artigo em Es | IBECS | ID: ibc-057988

RESUMO

El sistema hormonal de la vitamina D presenta múltiples e importantes relaciones con la función muscular, además de sus conocidos efectos sobre el metabolismo mineral. Tomados en conjunto estos datos resaltan la importancia del sistema hormonal de la vitamina D en la génesis de la fractura osteoporótica y en su reparación


The hormonal system of the vitamin D shows numerous and important relationships with the muscular function in addition to its known effects over the mineral metabolism. All these dates reflect the importance of the hormonal system of vitamin D in the generation of the osteoporotical fracture and in its reparation


Assuntos
Humanos , Vitamina D/metabolismo , Fenômenos Fisiológicos Musculoesqueléticos , Consolidação da Fratura/fisiologia , Músculo Esquelético/metabolismo , Deficiência de Vitaminas/metabolismo , Hiperparatireoidismo/fisiopatologia , Músculo Liso Vascular/metabolismo , Densidade Óssea/fisiologia
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