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Title of Journal: Mol Cell Biochem

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Abbravation: Molecular and Cellular Biochemistry

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Springer US

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DOI

10.1016/0300-483x(80)90040-2

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ISSN

1573-4919

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Smad2 protects against TGFβ1/Smad3mediated colla

Authors: Lei Zhang Changwei Liu Xiaoming Meng Cheng Huang Fengyun Xu Jun Li
Publish Date: 2014/10/29
Volume: 400, Issue: 1-2, Pages: 17-28
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Abstract

With structural similarity but functional diversity Smad2 and Smad3 interact with each other to mediate transforming growth factorβ TGFβtriggered signaling transduction However in the hepatic fibrosis the detailed roles of RSmads and interaction between Smad2 and Smad3 are still undefined In this setting we established a rat model of CCl4induced hepatic fibrosis in vivo and TGFβ1treated hepatic stellate cell model in vitro to detect whether Smad2 and Smad3 play distinct roles in mediating liver fibrogenesis Results indicated that both phosphorylation of Smad2 and Smad3 were detected in the hepatic stellate cells of liver fibrotic tissues and cells Furthermore In vitro data demonstrated that knockdown of Smad2 in human hepatic stellate cells increased expression of collagen I ColI tissue inhibitor of metalloproteinase1 TIMP1 whereas decreasing expression of the matrix metalloproteinases2MMP2 in presence of TGFβ1 compared with control group In contrast knockdown of Smad3 significantly reduced TGFβ1induced ColI production These findings were further evident by the results that overexpression of Smad2 attenuated the expression of ColI and TIMP1 but enhanced MMP2 whereas overexpression of Smad3 showed the opposite effect Furthermore Smad2 suppressed the phosphorylation and nuclear translocation of Smad3 which may protect against Smad3mediated fibrotic response Collectively Smad2 may be a potential therapeutic target for the treatment of hepatic fibrosis

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