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| Roles of Smad3 and Smad7 in rat pancreatic stellate cells activated by transforming growth factor-beta 1 |
| Zhu-Yin Qian, Quan Peng, Zheng-Wei Zhang, Long-An Zhou and Yi Miao |
Nanjing, China
Author Affiliations: Department of General Surgery, First Affiliated Hospital, Nanjing Medical University, Nanjing 210029, China (Qian ZY, Peng Q, Zhang ZW, Zhou LA and Miao Y)
Corresponding Author: Zhu-Yin Qian, PhD, Department of General Surgery, First Affiliated Hospital, Nanjing Medical University, Nanjing 210029, China (Tel: 86-25-83718836; Fax: 86-25-83724440; Email: qianzhusilver@163.com) |
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Abstract BACKGROUND: Pancreatic stellate cells (PSCs) play a major role in promoting pancreatic fibrosis. Transforming growth factor beta 1 (TGF-β1) 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-β1 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-β1 for 24 hours.
RESULTS: Smad7 expression was decreased in TGF-β1-activated PSCs (P<0.05) in a dose-dependent manner. When TGF-β1 concentration reached 10 ng/ml, the expression of p-Smad3, Smad3, and Smad7 was inhibited (P<0.05).
CONCLUSIONS: TGF-β1 promotes the expression of Smad3 and inhibits the expression of Smad7 during the activation of PSCs. In contrast, high-dose TGF-β1 downregulates the expression of Smad3 in completely activated PSCs.
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2010, Vol. 9 
