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Pro-inflammatory effect of transforming growth factor β1 in rat peritoneal mesothelial cells / 中华肾脏病杂志
Chinese Journal of Nephrology ; (12): 420-424, 2009.
Artigo em Chinês | WPRIM | ID: wpr-380752
ABSTRACT
Objective To investigate the pro-inflammatory effect of transforming growth factor β1 (TGF-β1) in rat peritoneal mesothelial cells (RPMCs) and its machanism. Methods TGF-β1-induced RPMCs model in vitro was established, and the expression of MCP-1 in the TGF-β1-induced RPMCs was observed. The intervention of Smad7 on the expression of MCP-1 and p38 signal proteins induced by TGF-β1 in RPMCs was explored as well as the intervention of p38 inhibitor SB203580 on the expression of MCP-1 induced by TGF-β1 in RPMCs. Results TGF-β1 could stimulate MCP-1 expression in RPMCs. Compared with control group, MCP-1 mRNA levels were significantly increased after 3 h treatment with TGF-β1 (P<0.05), peak MCP-1 induction occurred at 6 h (P<0.01), and the stimulatory effect of TGF-β1 persisted through 24 h (P<0.05). MCP-1 protein levels were significantly increased after 6 h treatment with TGF-β1(P<0.05), peak MCP-1 induction occurred at 48 h(P<0.01). Over-expressed Smad7 and p38 inhibitor could reduce the expression of MCP-1 induced by TGF-β1 (P<0.05). TGF-β1 could activate p38 signaling pathway, but over-expressed Smad7 could inhibit this role of TGF-β1. Compared with control group, the expression level of p-p38 was increased in TGF-β1-stimulated group. Compared with TGF-β1-stimulated group, the expression level of p-p38 was reduced in Smad7 gene transfer group. Conclusions TGF-β1-induced MCP-1 expression in rat peritoneal mesothelial cells is p38MAPK dependent.

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Tipo de estudo: Estudo prognóstico Idioma: Chinês Revista: Chinese Journal of Nephrology Ano de publicação: 2009 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Tipo de estudo: Estudo prognóstico Idioma: Chinês Revista: Chinese Journal of Nephrology Ano de publicação: 2009 Tipo de documento: Artigo