Smad3 和 Smad7 在转化生长因子-β 1 激活的大鼠胰腺星状细胞中的作用。
Roles of Smad3 and Smad7 in rat pancreatic stellate cells activated by transforming growth factor-beta 1.
机构信息
Department of General Surgery, First Affiliated Hospital, Nanjing Medical University, Nanjing 210029, China.
出版信息
Hepatobiliary Pancreat Dis Int. 2010 Oct;9(5):531-6.
BACKGROUND
Pancreatic stellate cells (PSCs) play a major role in promoting pancreatic fibrosis. Transforming growth factor beta 1 (TGF-beta1) is a critical mediator of this process. This study aimed to determine the expression of the Smad3 and Smad7 genes in the process of PSC activation, and explore the mechanisms of chronic pancreatitis.
METHODS
The expressions of Smad3 and Smad7 in PSCs before and after TGF-beta1 treatment were detected by reverse transcription-polymerase chain reaction and Western blotting analysis. Smad3 expression was detected in PSCs after treatment with 5 ng/ml of TGF-beta1 for 24 hours.
RESULTS
Smad7 expression was decreased in TGF-beta1-activated PSCs (P<0.05) in a dose-dependent manner. When TGF-beta1 concentration reached 10 ng/ml, the expression of p-Smad3, Smad3, and Smad7 was inhibited (P<0.05).
CONCLUSIONS
TGF-beta1 promotes the expression of Smad3 and inhibits the expression of Smad7 during the activation of PSCs. In contrast, high-dose TGF-beta1 downregulates the expression of Smad3 in completely activated PSCs.
背景
胰腺星状细胞（PSCs）在促进胰腺纤维化中起主要作用。转化生长因子β1（TGF-β1）是该过程的关键介质。本研究旨在确定 Smad3 和 Smad7 基因在 PSC 激活过程中的表达，并探讨慢性胰腺炎的发病机制。
方法
采用逆转录-聚合酶链反应和 Western blot 分析检测 TGF-β1 处理前后 PSCs 中 Smad3 和 Smad7 的表达。用 5ng/ml TGF-β1 处理 PSCs 24 小时后检测 Smad3 的表达。
结果
TGF-β1 激活的 PSCs 中 Smad7 表达呈剂量依赖性下降（P<0.05）。当 TGF-β1 浓度达到 10ng/ml 时，p-Smad3、Smad3 和 Smad7 的表达受到抑制（P<0.05）。
结论
TGF-β1 在 PSCs 的激活过程中促进 Smad3 的表达，抑制 Smad7 的表达。相反，高浓度 TGF-β1 下调完全激活的 PSCs 中 Smad3 的表达。
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