The involvement of p38 MAPK in transforming growth factor β1-induced apoptosis in murine hepatocytes
The involvement of p38 MAPK in transforming growth factor β1-induced apoptosis in murine hepatocytes
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DOI：
10.1038/sj.cr.7290072
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发表时间：
2001-06-01
期刊：
影响因子：
44.1
通讯作者：
Song, JG
中科院分区：
文献类型：
--
作者：
Liao, JH;Chen, JS;Song, JG
我们在这篇手稿中报道，TGF-β1 诱导 AML12 小鼠肝细胞凋亡，这与 p38 MAPK 信号通路的激活有关。 SB202190 是 p38 MAPK 的特异性抑制剂，强烈抑制 TGF-β1 诱导的细胞凋亡和 PAI-1 启动子活性。用 TGF-β1 处理细胞会激活 p38。此外，显性失活突变体p38的过度表达也减少了TGF-β1诱导的细胞凋亡。数据表明p38的激活参与TGF-β1介导的基因表达和细胞凋亡。
We reported in this manuscript that TGF-beta1 induces apoptosis in AML12 murine hepatocytes, which is associated with the activation of p38 MAPK signaling pathway. SB202190, a specific inhibitor of p38 MAPK, strongly inhibited the TGF-beta1-induced apoptosis and PAI-1 promoter activity. Treatment of cells with TGF-beta1 activates p38. Furthermore, over-expression of dominant negative mutant p38 also reduced the TGF-beta1-induced apoptosis. The data indicate that the activation of p38 is involved in TGF-beta1-mediated gene expression and apoptosis.