Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 1 de 1
Filtrar
Más filtros

Banco de datos
Tipo de estudio
Tipo del documento
País de afiliación
Intervalo de año de publicación
1.
J Cell Biochem ; 117(6): 1370-83, 2016 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-26538296

RESUMEN

The chemotactic migration of mesenchymal stem cells (MSCs) is fundamental for their use in cell-based therapies, but little is known about the molecular mechanisms that regulate their directed migration. MicroRNAs (miRNAs) participate in the regulation of a large variety of cellular processes. However, their roles in regulating the responses of MSCs to hepatocyte growth factor (HGF) remain elusive. Here, we found that microRNA-221 (miR-221) and microRNA-26b (miR-26b) were upregulated in MSCs subjected to HGF. Overexpression of miR-221 or miR-26b enhanced MSC migration through activation of PI3K/Akt signaling. Phosphatase and tensin homolog deleted on chromosome ten (PTEN) was identified as a potential target of miR-221 and miR-26b; overexpression of miR-221 or miR-26b decreased PTEN expression at both mRNA and protein levels. Overexpression of miR-221 or miR-26b in MSCs increased the phosphorylation of focal adhesion kinase (FAK), a downstream effector of PTEN, which regulates cell migration through assembly and distribution of focal adhesions (FAs), and more dot-like FAs were localized at the periphery of these cells. Altering miR-221 or miR-26b expression influenced the directed migration of MSCs toward HGF. Inhibition of miR-221 or miR-26b suppressed the phosphorylation of Akt and FAK and upregulated PTEN expression, which was partly restored by HGF treatment. Collectively, these results demonstrate that miR-221 and miR-26b participate in regulating the chemotactic response of MSCs toward HGF.


Asunto(s)
Quinasa 1 de Adhesión Focal/metabolismo , Factor de Crecimiento de Hepatocito/farmacología , Células Madre Mesenquimatosas/citología , MicroARNs/genética , Proteínas Proto-Oncogénicas c-akt/metabolismo , Animales , Movimiento Celular/efectos de los fármacos , Quimiotaxis/efectos de los fármacos , Perfilación de la Expresión Génica , Regulación de la Expresión Génica/efectos de los fármacos , Células Madre Mesenquimatosas/efectos de los fármacos , Ratas , Transducción de Señal
SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA