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IL-1#beta# stimulates #alpha#-smooth muscle actin expression through JNK/p38 signal pathway in cultured rat mesangial cells

Wang Yu, Li Xiaomei, Wang Haiyan

Renal Division,Department of Medicine,Peking University First Hospital,Peking University.Beijing 100034；China

Abstract

The results were compared between the groups stimulated by IL-1#beta# with or without PD98059 and SB203580, which are thought to block ERK and p38 pathway, respectively. Dominant-negative-JNKK plasmid was co-transfected in rMC to block JNK pathway. The spatial distribution of #alpha#-SMA and microfilament-like structure was observed by a confocal laser scanning microscope or an electric microscope. After 6 or 24h of incubation with IL-1#beta#, rMC underwent a phenotypic change, which was represented by up-regulation of #alpha#-SMA promoter activity and protein expression. An increase in #alpha#-SMA and microfilament-like structure was found around the cell nucleus. Block of JNK and/or p38 pathway greatly inhibited IL-1#beta#-induced #alpha#-SMA expression, and the block of p38 pathway also suppressed the basal level ofo #alpha#-SMA expression. In contrast, ERK pathway had no influence on the process.

Key words: Smooth muscle actins;Mesangial cell;Interleukin-1;Mitogen activated protein kinases

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Citing This Article：

Wang Yu, Li Xiaomei, Wang Haiyan. IL-1#beta# stimulates #alpha#-smooth muscle actin expression through JNK/p38 signal pathway in cultured rat mesangial cells. Acta Physiol Sin 2002; 54 (3): (in Chinese with English abstract).