转化生长因子-β/信号转导和转录激活因子信号通路阻断对肝星状细胞（HSCs）中miR-335、miR-150、miR-194、miR-27a和miR-199a表达谱的影响。
Effect of TGF-β/smad signaling pathway blocking on expression profiles of miR-335, miR-150, miR-194, miR-27a, and miR-199a of hepatic stellate cells (HSCs).
作者信息
Davoodian Parivash, Ravanshad Mehrdad, Hosseini Seyed Younes, Khanizadeh Sayyad, Almasian Mohammad, Nejati Zadeh Azim, Esmaiili Lashgarian Hamed
机构信息
Infectious and Tropical Diseases Research Center, Hormozgan University of Medical Sciences, Bandar Abbas, Iran.
Department of Virology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
出版信息
Gastroenterol Hepatol Bed Bench. 2017 Spring;10(2):112-117.
AIM
The aim of this study was to determine the effect of inhibition of TGF-β/smad signaling on the expression profiles of miR-335, miR-150, miR-194, miR-27a, miR-199a of hepatic stellate cells (HSCs).
BACKGROUND
Liver fibrosis is excessive deposition of extracellular matrix proteins due to ongoing inflammation and HSC activation that occurs in most types of chronic liver diseases. Recent studies have shown the importance of microRNAs in the pathogenesis of chronic liver diseases.
METHODS
In this study, for inhibition of TGF-β smad-signaling pathway, expressing Smad4 shRNA plasmids were transfected into HSCs. Subsequently, using Real Time-PCR, we measured the expression levels of miR-335, miR-150, miR-194, miR-27a and miR-199a.
RESULTS
Gene expression analysis showed that downregulation of Smad4 by vector Smad4shRNA significantly increased the expression levels of miR-335 (P<0.01) and miR-150 (P<0.001) and decreased the expression level of miR-27a (P<0.05).
CONCLUSION
The results of this study suggest that blocking TGF-β smad-signaling can also differentially modulate microRNA expression in support of activation and fibrogenesis of HSCs.
目的
本研究旨在确定抑制转化生长因子-β（TGF-β）/Smad信号通路对肝星状细胞（HSCs）中miR-335、miR-150、miR-194、miR-27a、miR-199a表达谱的影响。
背景
肝纤维化是由于大多数类型的慢性肝病中持续存在的炎症和肝星状细胞激活导致细胞外基质蛋白过度沉积。最近的研究表明微小RNA在慢性肝病发病机制中的重要性。
方法
在本研究中，为抑制TGF-β Smad信号通路，将表达Smad4短发夹RNA（shRNA）质粒转染到肝星状细胞中。随后，使用实时定量聚合酶链反应（Real Time-PCR）测量miR-335、miR-150、miR-194、miR-27a和miR-199a的表达水平。
结果
基因表达分析表明，载体Smad4shRNA使Smad4下调，显著增加了miR-335的表达水平（P<0.01）和miR-150的表达水平（P<0.001），并降低了miR-27a的表达水平（P<0.05）。
结论
本研究结果表明，阻断TGF-β Smad信号通路也可以差异性地调节微小RNA的表达，以支持肝星状细胞的激活和纤维化形成。
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