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1.
Allergol. immunopatol ; 48(1): 8-17, ene.-feb. 2020. ilus
Artigo em Inglês | IBECS | ID: ibc-186586

RESUMO

Introduction and objectives: LRBA deficiency is caused by loss of LRBA protein expression, due to either homozygous or compounds heterozygous mutations in LRBA. LRBA deficiency has been shown to affect vesicular trafficking and autophagy. To date, LRBA has been observed in the cytosol, Golgi apparatus and some lysosomes in LPS-stimulated murine macrophages. The objectives of the present study were to study the LRBA localization in organelles involved in vesicular traffic, phagocytosis, and autophagy in mononuclear phagocytes (MP). Materials and methods: We analyzed LRBA colocalization with different endosomes markets using confocal microscopy in MP. We used the autophagy inhibitors to determine the role of LRBA in formation, maturation or degradation of the autophagosome. Results: LRBA intracellular trafficking depends on the activity of the GTPase ADP ribosylation factor-1 (ARF) in MP. LRBA was identified in early, late endosomes but did not colocalize strongly with lysosomal markers. Although LRBA appears not to be recruited during the phagocytic cargo uptake, it greatly colocalized with the microtubule-associated protein 1A/1B-light chain 3 (LC3) under a steady state and this decreased after the induction of autophagy flux. Although the use of inhibitors of lysosome fusion did not restore the LRBA/LC3 colocalization, inhibitors of either early to late endosomes trafficking or PI3K pathway did. Conclusions: Taken together, our results show that LRBA is located in endomembrane system vesicles, mainly in the early and late endosomes. Although LRBA appears not to be involved in the phagocytic uptake, it is recruited in the early steps of the autophagy flux


No disponible


Assuntos
Proteínas Adaptadoras de Transdução de Sinal , Membrana Celular/metabolismo , Lipopolissacarídeos/farmacologia , Síndromes de Imunodeficiência/complicações , Diferenciação Celular , Endossomos , Microscopia Confocal/métodos , Autofagossomos , Fatores de Ribosilação do ADP , Fagocitose , Western Blotting , Sistema Fagocitário Mononuclear
2.
J. physiol. biochem ; 74(4): 579-589, nov. 2018. graf
Artigo em Inglês | IBECS | ID: ibc-179036

RESUMO

The main aim of this investigation was to study the regulatory roles of let-7b and miR-155-3p on the expression of inflammation-associated genes in monocytes, macrophages, and lipopolysaccharide (LPS)-activated macrophages (AcM). A second goal was to analyze the potential modulatory roles of different fatty acids, including oleic, palmitic, eicosapentaenoic (EPA), and docosahexaenoic (DHA), on the expression of these miRNAs in the three cell types. This hypothesis was tested in human acute monocytic leukemia cells (THP-1), which were differentiated into macrophages with 2-O-tetradecanoylphorbol-13-acetate (TPA) and further activated with LPS for 24 h. Monocytes, macrophages, and AcM were transfected with a negative control, or mimics for miR-155-3p and miR-let-7b-5p. The expression of both miRNAs and some proinflammatory genes was analyzed by qRT-PCR. Interestingly, let-7b mimic reduced the expression of IL6 and TNF in monocytes, and SERPINE1 expression in LPS-activated macrophages. However, IL6, TNF, and SERPINE1 were upregulated in macrophages by let-7b mimic. IL6 expression was higher in the three types of cells after transfecting with miR-155-3p mimic. Similarly, expression of SERPINE1 was increased by miR-155-3p mimic in monocytes and macrophages. However, TLR4 was downregulated by miR-155-3p in monocytes and macrophages. Regarding the effects of the different fatty acids, oleic acid increased the expression of let-7b in macrophages and AcM and also increased the expression of miR-155 in monocytes when compared with DHA but not when compared with non-treated cells. Overall, these results suggest anti- and proinflammatory roles of let-7b and miR-155-3p in THP-1 cells, respectively, although these outcomes are strongly dependent on the cell type. Noteworthy, oleic acid might exert beneficial anti-inflammatory effects in immune cells (i.e., non-activated and LPS-activated macrophages) by upregulating the expression of let-7b


No disponible


Assuntos
Humanos , Ácidos Graxos não Esterificados/metabolismo , Macrófagos/metabolismo , MicroRNAs/metabolismo , Monócitos/metabolismo , Diferenciação Celular , Ácidos Docosa-Hexaenoicos/metabolismo , Regulação para Baixo , Interleucina-6/agonistas , Interleucina-6/antagonistas & inibidores , Interleucina-6/genética , Lipopolissacarídeos/toxicidade , Ativação de Macrófagos , MicroRNAs/química
3.
An Real Acad Farm ; 84(2): 154-163, abr.-jun. 2018.
Artigo em Espanhol | IBECS | ID: ibc-178053

RESUMO

La mayor parte de los tumores están estructurados jerárquicamente, siendo la población de células madre del cáncer la encargada de iniciar y mantener el tumor. Estas células madre del cáncer, debido a sus similitudes con las células madre sanas, tienen capacidad de auto-renovación y diferenciación. Existe un balance altamente regulado que controla ambos procesos. De forma que la eliminación de la auto-renovación directamente o la inducción terminal de diferenciación producen la eliminación de las células madre del cáncer y, por lo tanto, la capacidad de mantenimiento y regeneración de la neoplasia. El desarrollo de dos plataformas distintas para buscar compuestos de pequeño tamaño bioactivos que induzcan la diferenciación terminal de las células madre del cáncer ha permitido identificar distintos fármacos con potencial acción neoplásica. Estas plataformas están basadas en cribados de alto rendimiento y alto contenido usando un sistema de células madre embrionarias transformadas y un análisis bioinformático in silico. Usando la leucemia mieloide aguda como modelo de tumor jerárquico, estos compuestos se estudiado ex vivo y in vivo y se han optimizado para su evaluación clínica. Estas plataformas de descubrimiento de fármacos se han validado como una nueva aproximación experimental para identificar nuevos fármacos con actividad diferenciadora anti-tumoral


Most of the tumors are hierarchically organized, with a cellular subpopulation of cancer stem cells in the apex. This population is responsible for the initiation and maintenance of the tumor. Due to their "stem cell"-like properties, cancer stem cells display self-renewal and differentiation potential, both properties are tightly regulated. Thus, direct inhibition of self-renewal or induction of terminal differentiation will eradicate cancer stem cells and, thus, the maintenance and regeneration capacity of the neoplasia will be eliminated. Two distinct drug discovery platforms were developed to identify small bioactive compounds that induce terminal differentiation of cancer stem cells. These platforms are based on highthroughput and high-content screenings using a transformed embryonic stem cell system and an in silico bioinformatics analysis. Using acute myeloid leukemia as a hierarchically organized tumor model, these compounds were studied ex vivo and in vivo and optimized for clinical settings. These platforms have been validated as a new experimental approach to identify differentiating-inducing drugs as anti-neoplastic compounds


Assuntos
Humanos , Preparações Farmacêuticas , Neoplasias/tratamento farmacológico , Células-Tronco , Sistema Hematopoético , Diferenciação Celular , Autorrenovação Celular , Camundongos Endogâmicos , Antígenos CD34 , ADP-Ribosil Ciclase 1
5.
Rev. iberoam. fertil. reprod. hum ; 34(1): 34-43, ene.-mar. 2017.
Artigo em Espanhol | IBECS | ID: ibc-162673

RESUMO

Durante mucho tiempo se ha intentado hallar las primeras diferencias entre células que ocurren durante el desarrollo preimplantacional en el embrión de mamífero, y que posteriormente darán lugar a diferentes destinos celulares. En los últimos años los estudios han demostrado que este proceso está regulado por diferencias en interacciones célula-célula, expresión génica y el microambiente de cada célula, en vez de por la división diferencial de determinantes maternos como pasa en otras especies. Sin embargo como aparecen estas diferencias en un primer momento y como regulan los factores moleculares y celulares implicados en la diferenciación celular es una pregunta por resolver. La escasez de material y las limitaciones éticas complican el estudio en embriones humanos. Poco a poco los nuevos avances en técnicas de imagen y análisis de transcriptómica de una única célula proveen nuevos conocimientos que ayudarán a resolver las dudas que se plantean hoy en día (AU)


For a long time, it has been tried to find the first differences between cells taking place during preimplantational development of the mammalian embryo, arising different cell fates. Instead of differential divisions of maternal determinants as occurs in other species. It has been shown that this process is regulated by differences in cell to cell interactions, gene expression and individual cell microenvironment. However, how this differences at first appear and how molecular and cellular factors involved in differentiation are regulated, is still unknown. Material shortage and ethical limitations complicate the study on human embryos. Gradually the new advances in imaging techniques and transcriptome analysis of a single cell provide new insights that will help to solve questions that arise today (AU)


Assuntos
Humanos , Diagnóstico Pré-Implantação/métodos , Desenvolvimento Embrionário/fisiologia , Padronização Corporal/fisiologia , Células-Tronco Totipotentes/fisiologia , Polaridade Celular/fisiologia , Expressão Gênica/genética , Fase de Clivagem do Zigoto/fisiologia , Diferenciação Celular/genética
6.
Rev. neurol. (Ed. impr.) ; 64(supl.1): s45-s50, 2017. ilus
Artigo em Espanhol | IBECS | ID: ibc-163033

RESUMO

La neuroplasticidad es la capacidad biológica que tiene el sistema nervioso de modificar su estructura y función para adaptarse a las variaciones del entorno, tanto fisiológicas como patológicas. Sus principales consecuencias fisiológicas son el aprendizaje y la memoria, y las patológicas, la rehabilitación neurológica. El continuo cambio y la fragilidad inicial del cerebro en desarrollo hacen especialmente plásticos los períodos embrionario y fetal (lo que se conoce como neuroplasticidad del desarrollo). Ahora bien, la reducción progresiva de la plasticidad nunca es total, permaneciendo a lo largo de toda la vida la capacidad de modificar los circuitos cerebrales en respuesta a nuevos aprendizajes (neuroplasticidad adaptativa) o a lesiones cerebrales (neuroplasticidad reactiva). El principal mecanismo neurobiológico de la neuroplasticidad es la formación de contactos sinápticos entre neuronas. Los trastornos del neurodesarrollo están asociados a anomalías funcionales del cerebro, muchas veces derivadas de la falta de capacidad adaptativa o reactiva del cerebro para modificar los circuitos malformados o dañados por anomalías genéticas o ambientales. Clásicamente se asocian con la aparición de discapacidad intelectual y enfermedades mentales. Esta revisión trata sobre el desarrollo de la neuroplasticidad cerebral y sus mecanismos neurobiológicos. También se analizan algunos de los procesos celulares y moleculares que están implicados en su desarrollo normal y las posibles consecuencias derivadas de sus alteraciones (AU)


Neuroplasticity is the biological capacity of the nervous system to modify its structure and functioning to adapt to both physiological and pathological variations in the environment. Its main physiological consequences are learning and memory, and its pathological outcome is neurological rehabilitation. The continuous change and initial fragility of the developing brain make the embryonic and foetal periods especially plastic (what is known as developmental neuroplasticity). The progressive reduction in plasticity, however, is never complete and the capacity to modify the brain circuits in response to new learning (adaptive neuroplasticity) or brain injuries (reactive neuroplasticity) remains throughout the individual’s entire lifespan. The main neurobiological mechanism underlying neuroplasticity is the formation of synaptic contacts between neurons. Neurodevelopmental disorders are associated to functional anomalies of the brain, often derived from the lack of adaptive or reactive capacity of the brain to modify circuits that are malformed or damaged by genetic or environmental anomalies. They are traditionally associated with the appearance of intellectual disability and mental illnesses. This review deals with the development of the neuroplasticity of the brain and its neurobiological mechanisms. Some of the cellular and molecular processes involved in its normal development are also examined, together with the possible consequences deriving from alterations affecting them (AU)


Assuntos
Humanos , Criança , Deficiências da Aprendizagem/complicações , Deficiências da Aprendizagem/epidemiologia , Plasticidade Neuronal/fisiologia , Prosencéfalo/fisiologia , Diferenciação Celular/fisiologia , Cérebro/crescimento & desenvolvimento , Cérebro/fisiologia
7.
J. physiol. biochem ; 72(4): 689-697, dic. 2016. tab, graf
Artigo em Inglês | IBECS | ID: ibc-168376

RESUMO

The balance of ATP production and consumption is reflected in adenosine monophosphate (AMP) and nicotinamide adenine dinucleotide (NAD) content and has been associated with phenotypic plasticity in striated muscle. Some studies have suggested that AMPK-dependent plasticity may be an indirect consequence of increased NAD synthesis and SIRT1 activity. The primary goal of this study was to assess the interaction of AMP- and NAD-dependent signaling in adaptation of C2C12 myotubes. Changes in myotube developmental and metabolic gene expression were compared following incubation with 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) and nicotinamide mononucleotide (NMN) to activate AMPK- and NAD-related signaling. AICAR showed no effect on NAD pool or nampt expression but significantly reduced histone H3 acetylation and GLUT1, cytochrome C oxidase subunit 2 (COX2), and MYH3 expression. In contrast, NMN supplementation for 24 h increased NAD pool by 45 % but did not reduce histone H3 acetylation nor promote mitochondrial gene expression. The combination of AMP and NAD signaling did not induce further metabolic adaptation, but NMN ameliorated AICAR-induced myotube reduction. We interpret these results as indication that AMP and NAD contribute to C2C12 differentiation and metabolic adaptation independently (AU)


No disponible


Assuntos
Animais , Camundongos , Adaptação Fisiológica , Transdução de Sinais , NAD/metabolismo , Mioblastos/metabolismo , Monofosfato de Adenosina/metabolismo , Acetilação , Linhagem Celular , Diferenciação Celular , Aminoimidazol Carboxamida , Complexo IV da Cadeia de Transporte de Elétrons , Cadeias Pesadas de Miosina , Transportador de Glucose Tipo 1 , Mononucleotídeo de Nicotinamida/farmacologia , Ribonucleotídeos/farmacologia
8.
Int. microbiol ; 19(2): 81-90, jun. 2016. ilus
Artigo em Inglês | IBECS | ID: ibc-158062

RESUMO

All living organisms have acquired the outstanding ability to overcome the limitations imposed by changeable environments through the gain of genetic traits over years of evolution and the tendency of individuals to associate in communities. The complementation of a singular weakness, the deployment of reinforcement for the good of the community, the better use of resources, or effective defense against external aggression are advantages gained by this communal behavior. Communication has been the cohesive element prompting the global responses that promote efficiency in two features of any community: specialization in differentiated labor and the spatio-temporal organization of the environment. These principles illustrate that what we call human ecology also applies to the cellular world and is exemplified in eukaryotic organisms, where sophisticated cell-to-cell communication networks coordinate cell differentiation and the specialization of multiple tissues consisting of numerous cells embedded in a multifunctional extracellular matrix. This sophisticated molecular machinery appears, however, to be invented by the ‘simple’ but still fascinating bacteria. What I will try to expand in the following sections are notions of how ‘single prokaryotic cells’ organize a multicellular community (AU)


No disponible


Assuntos
Biota/fisiologia , Células Procarióticas/microbiologia , Diferenciação Celular/fisiologia , Fenômenos Fisiológicos Bacterianos , Matriz Extracelular/ultraestrutura , Biofilmes/crescimento & desenvolvimento
9.
Rev. osteoporos. metab. miner. (Internet) ; 8(1): 40-44, ene.-mar. 2016. ilus
Artigo em Espanhol | IBECS | ID: ibc-151233

RESUMO

Los micro-ARN (miRs) son pequeñas moléculas de ARN no codificantes que regulan la expresión génica a nivel post-transcripcional. Generalmente actúan sobre la expresión genética mediante el silenciamiento o degradación de los ARNm, y están implicados en la regulación de varios procesos biológicos, como la diferenciación celular, la proliferación, la apoptosis y en el desarrollo embrionario y tisular. Actualmente son un importante foco de interés para el estudio de diversas enfermedades como el cáncer o la diabetes mellitus tipo 2. A nivel del metabolismo óseo, están surgiendo diversos miRs implicados en su regulación, abriendo un campo de investigación importante para identificar nuevos biomarcadores para el diagnóstico de la enfermedad osteoporótica, de su evolución, así como para diseñar nuevas terapias farmacológicas (AU)


Micro-RNAs (miRs) are small non-coding RNA molecules that regulate gene expression at post-transcriptional level. Generally, they act on gene expression by silencing or degrading mRNAs, and are involved in regulating various biological processes, such as cell differentiation, proliferation, apoptosis and in embryonic and tissue development. They are currently a major focus of interest in the study of various diseases such as cancer or type 2 diabetes mellitus. At level of bone metabolism, various miRs are emerging that are involved in their regulation, opening an important research field to identify new biomarkers for diagnosis of osteoporosis and its development, and to design new drug therapies (AU)


Assuntos
Humanos , MicroRNAs , Osteoporose/genética , Epigenômica , Epigênese Genética , Biomarcadores/análise , Marcadores Genéticos , Processamento Pós-Transcricional do RNA/genética , Diferenciação Celular/genética , Apoptose/genética
10.
Clin. transl. oncol. (Print) ; 17(11): 847-855, nov. 2015. tab, ilus
Artigo em Inglês | IBECS | ID: ibc-143454

RESUMO

Salivary gland myoepithelial carcinoma (MC) or malignant myoepithelioma is a rare entity. MC usually presents as a slow-growing painless mass arising in the parotid gland, but may involve other salivary glands. This tumour may be particularly locally aggressive, but its clinical and biological features are not yet fully understood. MC may arise from pre-existing benign lesions, such as pleomorphic adenomas or benign myoepitheliomas, or may arise de novo. It usually affects patients over 50 years old, with no gender preference. Because it is often asymptomatic, the presentation and diagnosis can be delayed by months, even years. The current WHO classification considers MC to be an intermediate- to high-grade malignancy. Other published data suggest it is likely to be a high-grade neoplasm, consistent with its aggressive behaviour. Its epidemiology, histopathological features, immunohistochemical profile, clinical behaviour and optimal management are not well understood. Following review of the current literature we aim to address these (AU)


No disponible


Assuntos
Feminino , Humanos , Masculino , Glândulas Salivares/imunologia , Glândulas Salivares/patologia , Neoplasias das Glândulas Salivares/diagnóstico , Imuno-Histoquímica/instrumentação , Imuno-Histoquímica/métodos , Imuno-Histoquímica , Mioepitelioma/complicações , Mioepitelioma/diagnóstico , Carcinoma/complicações , Carcinoma/diagnóstico , Mioepitelioma/patologia , Diferenciação Celular , Diagnóstico Diferencial , Neoplasias das Glândulas Salivares/tratamento farmacológico , Neoplasias das Glândulas Salivares/radioterapia
12.
Nutr. hosp ; 32(2): 545-555, ago. 2015. ilus, tab
Artigo em Espanhol | IBECS | ID: ibc-139985

RESUMO

La principal función de los adipocitos es el almacenamiento de lípidos cuando hay exceso de energía y la movilización de la misma cuando hay deficiencia. Una de las características de la obesidad es el aumento de la cantidad y el tamaño de los adipocitos, lo que implica la diferenciación de preadipocitos (PAD). El tejido adiposo (TA) tiene su origen en la etapa prenatal y puede seguir expandiéndose durante la vida adulta a partir de células precursoras, ya que los adipocitos maduros no pueden multiplicarse por división celular. El presente estudio proveerá información reciente de los eventos que se producen durante el origen y diferenciación de los PAD, así como los factores implicados en la regulación de la adipogénesis y los mecanismos que regulan las funciones fisiológicas del TA (AU)


The main function of the adipocyte is lipid storage when there is a positive energy balance and lipid release when there is and energy deficiency. One characteristic of obesity is an increase in the number and size of adipocytes, which implies pre adipocyte (PAD) differentiation. The adipose tissue (AT) has its origins in the prenatal stage and may continue to expand during adulthood from precursor cells since mature adipocytes cannot multiply by cell division. This study provide updates on the events that occur during the origin and differentiation of PAD, the factors involved in the regulation of adipogenesis and mechanisms that regulate physiological functions of AT (AU)


Assuntos
Feminino , Humanos , Masculino , Adipogenia , Tratamento Farmacológico/organização & administração , Fitoterapia/métodos , Adipócitos , Células-Tronco , Diferenciação Celular , Alcaloides/uso terapêutico , Etnofarmacologia/métodos , Receptores de Citocinas , Receptores de Citocinas/uso terapêutico , Inflamação/tratamento farmacológico , Obesidade/tratamento farmacológico , Fármacos Antiobesidade/efeitos adversos , Fármacos Antiobesidade/uso terapêutico , Nelumbo
13.
Eur. j. anat ; 19(2): 189-195, abr. 2015. ilus, tab
Artigo em Inglês | IBECS | ID: ibc-141209

RESUMO

Caspases are proteases primarily involved in the process of apoptosis; however, caspases can exert non-apoptotic functions. The purpose of this work was to use immunohistochemistry to analyse the expression sites of caspase-2 during normal mouse cephalic development and in embryos exposed to irradiation. Control embryos from embryonic day 9 (E9) to E17 were analysed, and E9 and 10 irradiated embryos were removed and observed after administration of 2 Gy irradiation at embryonic day 9. Surprisingly, not only apoptotic cells expressed caspase-2. In addition, numerous cell populations in normal and experimental embryos displayed transient but intense caspase-2 immunoreactivity, with nuclear and cytoplasmic localisation. This immunoreactivity was not observed with caspase-3 and -9 antibodies. Cranial neural crest cells, premuscular blastemata, cartilage, teeth, the heart, the eye and some other structures displayed caspase-2 expression, with progressive changes during embryonic development. These changing patterns evoke progressive waves of cell differentiation in specific cell populations. Little is known regarding the non-apoptotic functions of caspase-2. Despite the difficulty in understanding the role of this protease during cell differentiation, the fact that caspase-2 is known to prevent DNA damage and to protect the cell cycle could be closely associated with our observations, which point to the need for further research, particularly in caspase-2 knockout mice


No disponible


Assuntos
Animais , Camundongos , Caspase 2/análise , Encéfalo/crescimento & desenvolvimento , Imuno-Histoquímica/métodos , Diferenciação Celular , Camundongos/embriologia
14.
Trauma (Majadahonda) ; 26(1): 4-10, ene.-mar. 2015. ilus
Artigo em Espanhol | IBECS | ID: ibc-138592

RESUMO

Objetivo: Generar células madre mesenquimales humanas (MSCs) modificadas para optimizar su potencial de diferenciación osteogénica, destinadas a su empleo en implantes cerámicos para regeneración ósea. Material y método: Se emplearon ratones inmunodeficientes NOD/SCID (3-6 ratones por condición experimental y ensayo) y se generaron vectores lentivirales basados en la recombinasa Cre, que sobreexpresan el factor regulador del proceso osteogénico Dlx5 (o la proteína fluorescente GFP como control) de forma autolimitada en el tiempo. Estos vectores se utilizaron para transducir hMSCs, y su potencial osteogénico se analizó in vitro e in vivo en un modelo de formación de hueso heterotópico en ratón. Resultados: Las hMSCs transducidas con los vectores que expresan Dlx5 de forma autolimitada fueron capaces de diferenciarse eficientemente a hueso de forma espontánea, de manera similar a las hMSCs control en presencia del factor osteoinductor BMP-2. Conclusión: Hemos desarrollado un sistema de modificación de hMSCs para aumentar su potencial osteogénico que consiste en un vector lentiviral que expresa el factor osteoinductor Dlx5 de forma autolimitada. Las hMSCs modificadas diferencian a hueso de manera eficiente, tanto in vitro como in vivo (AU)


Objective: This article proposes the generation of modified human mesenchymal stem cells (hMSCs) for optimizing their osteogenic differentiation potential, in order to be employed in ceramic implants for bone regeneration. Material and method: We have generated lentiviral vectors based on Cre recombinase, which lead to overexpression of a regulatory factor of osteogenic process, Dlx5 (or GFP fluorescent protein as a control), in a selflimited fashion. We have transduced hMSCs with these vectors, and we have analyzed their osteogenic potential both in vitro and in vivo in a model of heterotopic bone formation in mice. For this purpose we have used immunodeficient NOD/SCID mice (3-6 mice per condition and experiment). Results: hMSCs transduced with self-limited Dlx5-expressing vectors efficiently differentiate into bone in vitro and in vivo, similar to control hMSCs in the presence of osteoinductive factor BMP-2. Conclusion: We have developed a system to modify hMSCs in order to improve their osteogenic potential. This system consists of a lentiviral vector which expresses osteoinductive factor Dlx5 in a self-limited fashion. Modified hMSCs efficiently differentiate into bone, both in vitro and in vivo (AU)


Assuntos
Animais , Feminino , Masculino , Camundongos , Células-Tronco/classificação , Células-Tronco/fisiologia , Transplante de Células-Tronco/métodos , Regeneração Óssea/fisiologia , Lentivirus/isolamento & purificação , Terapia Baseada em Transplante de Células e Tecidos/métodos , Terapia Baseada em Transplante de Células e Tecidos , Terapia Baseada em Transplante de Células e Tecidos/veterinária , Doenças Ósseas/terapia , Doenças Ósseas/veterinária , Pesquisa com Células-Tronco , Diferenciação Celular/fisiologia , Terapia Baseada em Transplante de Células e Tecidos/instrumentação , Terapia Baseada em Transplante de Células e Tecidos/normas , Terapia Baseada em Transplante de Células e Tecidos/tendências
15.
Reumatol. clín. (Barc.) ; 10(6): 389-395, nov.-dic. 2014. ilus
Artigo em Espanhol | IBECS | ID: ibc-128366

RESUMO

La fibrodisplasia osificante progresiva es la causa más grave de osificación ectópica en humanos. Se caracteriza por malformaciones esqueléticas congénitas y placas de hueso maduro (endocondral) en el músculo y en otras estructuras ricas en tejido conjuntivo. Se produce por una mutación espontánea en el gen del receptor de la activina A tipo I, similar a la activina-cinasa-2. A raíz de este hallazgo, se han producido importantes avances en el conocimiento de su base molecular y celular. Además de permitir una mejor comprensión de los mecanismos que gobiernan la osificación, evidencias recientes indican que la alteración primordial radica en mecanismos básicos de la diferenciación celular que son clave en varias vías fisiológicas y en la génesis de enfermedades de gran impacto. En el presente artículo, resumimos los últimos avances con implicaciones que trascienden los límites de esta devastadora enfermedad para postularse como un nuevo modelo dentro de la fisiopatología humana (AU)


Fibrodysplasia ossificans progressiva is the most severe and disabling disorder of ectopic ossification in humans. It is characterized by congenital skeletal abnormalities in association with extraskeletal widespread endochondral osteogenesis. Virtually all patients show the same mutation in the «activin A type-I/activin-like kinase-2» receptor encoding gene. As a result of this discovery there have been significant advances in the knowledge of the cellular and molecular basis of the disease. Besides allowing a better understanding of ossification process, recent evidence indicates that the primary disturbance lies within basic mechanisms of cell differentiation that are key in several physiological pathways and in the genesis of diseases with a major impact on health. In this article we summarize these breakthroughs, with implications that go beyond the limits of this devastating disease to insinuate a new model of human pathophysiology (AU)


Assuntos
Humanos , Masculino , Feminino , Miosite Ossificante/epidemiologia , Miosite Ossificante/prevenção & controle , Proteína Morfogenética Óssea 1/análise , Proteína Morfogenética Óssea 1 , Mutação/genética , Diferenciação Celular/genética , Doenças Musculoesqueléticas/complicações , Doenças Musculoesqueléticas/diagnóstico , Doenças Musculoesqueléticas/genética , Disgenesia da Tireoide/complicações , Disgenesia da Tireoide
16.
J. physiol. biochem ; 70(3): 781-789, sept. 2014.
Artigo em Inglês | IBECS | ID: ibc-127322

RESUMO

MicroRNAs (miRNAs) are noncoding RNAs involved in the regulation of the diverse biological processes such as metabolism, proliferation, and cell cycle, in addition to regulation of differentiation. So far, some miRNAs have been recognized to have important role in regulating hepatic functions. Statistically, let-7f has been revealed as a negative regulator of hepatic differentiation. In the present study, we investigated the effect of let-7f on hepatic differentiation of human adipose tissue-derived stem cells (hADSCs). hADSCs were transduced with recombinant lentivirus containing human inhibitor let-7 f. The expression of hepatocyte nuclear factors alpha (HNF4a), albumin (ALB), alpha fetoprotein (AFP), cytokeratin 18 (CK18), and cytokeratin 19 (CK19) was evaluated using quantitative real-time PCR (qRT-PCR). Immunocytochemistry was used to investigate the expression levels of the hepatocyte markers including ALB, AFP, and HNF4a, and biochemical analysis was implemented for hepatic function, glycogen deposition, and urea secretion. qRT-PCR showed significant upregulation in HNF4a, ALB, AFP, CK18, and CK19 expression in cells transduced with let-7f inhibitor lentiviruses. Moreover, positive staining was detected for ALB, AFP, and HNF4a using immunocytochemistry. Urea production and glycogen deposits were also found in the treated cells, the two specific features of the hepatic cells. Therefore, let-7f silencing led to the increased expression of the hepatocyte-specific factors and the accelerated hADSCs hepatic differentiation. Summing all these finding together, our present report has provided evidences that inhibition of let-7f would facilitate induction of hADSCs into hepatocyte-like cells and possibly in regenerative therapy of the liver disease in a wider spectrum


No disponible


Assuntos
Humanos , Tecido Adiposo/citologia , Células-Tronco/fisiologia , Diferenciação Celular/fisiologia , MicroRNAs , Fibronectinas , Fator 1-alfa Nuclear de Hepatócito , alfa-Fetoproteínas , Queratinas , Albuminas , Diferenciação Celular
17.
Int. microbiol ; 17(2): 75-80, jun. 2014. ilus
Artigo em Inglês | IBECS | ID: ibc-127301

RESUMO

Streptomycetes are mycelium-forming bacteria that produce two thirds of the clinically relevant secondary metabolites. Despite the fact that secondary metabolite production is activated at specific developmental stages of the Streptomyces spp. life cycle, different streptomycetes show different behaviors, and fermentation conditions need to be optimized for each specific strain and secondary metabolite. Cell-encapsulation constitutes an interesting alternative to classical fermentations, which was demonstrated to be useful in Streptomyces, but development under these conditions remained unexplored. In this work, the influence of cell-encapsulation in hyphae differentiation and actinorhodin production was explored in the model Streptomyces coelicolor strain. Encapsulation led to a delay in growth and to a reduction of mycelium density and cell death. The high proportion of viable hyphae duplicated extracellular actinorhodin production in the encapsulated cultures with respect to the non-encapsulated ones (AU)


No disponible


Assuntos
Streptomyces coelicolor/ultraestrutura , Diferenciação Celular , Morte Celular , Micélio/ultraestrutura , Antibacterianos/farmacocinética
18.
J. investig. allergol. clin. immunol ; 24(1): 6-22, ene.-feb. 2014. ilus, tab
Artigo em Inglês | IBECS | ID: ibc-119149

RESUMO

Expression of selected genes in hematopoietic stem cells has been identified as a regulator of differentiation of B cells in the liver and bone marrow. Moreover, naïve B cells expressing surface immunoglobulin need other types of genes for antigen-dependent development in secondary lymphoid organs. Many advanced molecular mechanisms underlying primary antibody deficiencies in humans have been described. We provide an overview of the mutations in genes known to be involved in B-cell development and their clinical consequences (AU)


Se ha identificado la expresión de genes seleccionados en las células pluripotenciales de médula ósea como reguladores de la diferenciación de las células B en el hígado y en médula ósea. Sin embargo, las células B naïve que expresan inmunoglubulinas de superficie, necesitan otros tipos de genes para su desarrollo en los órganos linfoides secundarios dependienteS de antígeno. Se han descrito muchos mecanismos moleculares avanzados que subrayan las inmunodeficiencias en humanos y esta revisión constituye una visión general de la mutación en todos los genes conocidos involucrados en el desarrollo de las células B y sus consecuencias clínicas (AU)


Assuntos
Humanos , Linfócitos B , Diferenciação Celular , Expressão Gênica , Fenótipo , Doenças Genéticas Inatas , Agamaglobulinemia/genética
19.
Arch. Soc. Esp. Oftalmol ; 89(1): 10-16, ene. 2014. graf, ilus, tab
Artigo em Espanhol | IBECS | ID: ibc-129248

RESUMO

OBJETIVO: Evaluar diferentes cultivos primarios de conjuntiva humana enriquecidos con suero fetal bovino, suero autólogo y suero autólogo rico en plaquetas, sobre un soporte de membrana amniótica humana y cápsula anterior del cristalino. MÉTODOS: Ciento cuarenta y ocho explantes de conjuntiva humana fueron cultivados en CnT50® enriquecido con 1, 2,5, 5 y 10% en suero fetal bovino, suero autólogo y suero autólogo rico en plaquetas. Las muestras de conjuntivales fueron incubadas a 37 °C, 5% CO2 y 95% HR, durante 3 semanas. RESULTADOS: Todos los cultivos primarios tuvieron el fenotipo típico de las células epiteliales de la conjuntiva. Los cultivos mostraron células secretoras MUC5AC-positiva, células conjuntivales CK19-positiva y células conjuntivales no secretoras MUC4-positiva, pero sin fenotipo corneal (CK3-negativa) ni fibroblastos (CD90-negativa). CONCLUSIONES: Las células epiteliales progenitoras de la conjuntiva se mantuvieron en todos los cultivos, por lo que un cultivo celular en CnT50® enriquecido con suero autólogo entre el 1 y 5% sobre membrana amniótica humana puede proporcionar la mejor información de la diferenciación de las células epiteliales para la reconstrucción de la superficie conjuntival


OBJECTIVE: To evaluate primary cultures from human conjunctiva supplemented with fetal bovine serum, autologous serum, and platelet-rich autologous serum, over human amniotic membrane and lens anterior capsules. METHODS: One-hundred and forty-eight human conjunctiva explants were cultured in CnT50® supplemented with 1, 2.5, 5 and 10% fetal bovine serum, autologous serum and platelet-rich autologous serum. Conjunctival samples were incubated at 37 °C, 5% CO2 and 95% HR, for 3 weeks. RESULTS: The typical phenotype corresponding to conjunctival epithelial cells was present in all primary cultures. Conjunctival cultures had MUC5AC-positive secretory cells, K19-positive conjunctival cells, and MUC4-positive non-secretory conjunctival cells, but were not corneal phenotype (cytokeratin K3-negative) and fibroblasts (CD90-negative). CONCLUSIONS: Conjunctiva epithelial progenitor cells were preserved in all cultures; thus, a cell culture in CnT50® supplemented with 1 to 5% autologous serum over human amniotic membrane can provide better information of epithelial cell differentiation for the conjunctival surface reconstruction


Assuntos
Humanos , Técnicas de Cultura de Tecidos/métodos , Túnica Conjuntiva/fisiologia , Diferenciação Celular/fisiologia , Meios de Cultura
20.
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
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