Smad2 and Smad3 as mediators of the response of adventitial fibroblasts induced by transforming growth factor β1

被引：32

作者：

Ren, Min ^{[1
]}

Wang, Bo ^{[1
]}

Zhang, Jidong ^{[1
]}

Liu, Ping ^{[3
]}

Lv, Yijing ^{[1
]}

Liu, Guilin ^{[4
]}

Jiang, Hong ^{[2
]}

Liu, Fenye ^{[5
]}

机构：

[1] Shandong Univ, Qilu Hosp, Dept Tradit Chinese Med, Jinan 250012, Shandong, Peoples R China

[2] Shandong Univ, Qilu Hosp, Lab Cardiovasc Remodeling & Funct Res, Jinan 250012, Shandong, Peoples R China

[3] Shandong Univ, Hosp 2, Dept Hlth Management, Jinan 250033, Shandong, Peoples R China

[4] Shandong Acad Med Sci, Dept Med, Jinan 250062, Shandong, Peoples R China

[5] Shandong Prov Hosp, Dept Tradit Chinese Med, Jinan 250021, Shandong, Peoples R China

来源：

MOLECULAR MEDICINE REPORTS | 2011年 / 4卷 / 03期

基金：

中国国家自然科学基金;

关键词：

adventitial fibroblasts; transforming growth factor beta 1; Smad2; Smad3; MUSCLE ACTIN EXPRESSION; HEPATIC STELLATE CELLS; MYOFIBROBLAST TRANSDIFFERENTIATION; GENE-TRANSFER; COLLAGEN; DIFFERENTIATION; ACTIVATION; FIBROSIS; PROTEIN; HYPERTENSION;

D O I：

10.3892/mmr.2011.458

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 [肿瘤学];

摘要：

Transforming growth factor beta 1 (TGF-beta 1) is a known pleiotropic growth factor in cell proliferation, migration and phenotypic transition. Fibroblasts are considered the most reactive in the vascular wall. We aimed to explore the effect and mechanism of TGF-beta 1 on aortal adventitial fibroblasts (AFs) induced by TGF-beta 1. AFs were cultured in vitro by tissue explains. After stimulation by TGF-beta 1 and treatment with small interfering RNA (siRNA)-Smad2 and siRNA-Smad3, MTT and the transwell chamber techniques were used for assessing AF proliferation and migration. The expression of phospho (pho)-Smad2, pho-Smad3, Smad7, a-smooth muscle actin (SMA) and collagen I and III were evaluated by Western blot analysis and real-time RT-PCR. After stimulation by TGF-beta 1 for 24 h, the proliferation and migration of treated AFs were higher compared to those of untreated AFs, as was the expression of Smad2, Smad3, pho-Smad2, pho-Smad3, SMA and collagen I and III (P < 0.05), but not Smad7 (P > 0.05). Knockdown of Smad2 and Smad3 inhibited proliferation and migration of AFs and down-regulated the expression of SMA and collagen I and III (P < 0.05). TGF-beta 1 plays a key role in remodeling processes by contributing to the proliferation, migration and phenotypic modulation of AFs and collagen composition. The mechanism may be related to both the Smad2 and Smad3 signaling pathways.

引用

页码：561 / 567

页数：7

共 39 条

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