菱形
细胞生物学
肌动蛋白解聚因子
罗亚
分子生物学
MAPK/ERK通路
转染
p38丝裂原活化蛋白激酶
生物
磷酸化
信号转导
化学
肌动蛋白细胞骨架
细胞骨架
细胞
基因
生物化学
作者
Chloé Leduc,Lauren Sobilo,Hechmi Toumi,Philippe Mondon,Éric Lespessailles,Fédéric Ossant,Robin Kurfürst,Chantal Pichon
标识
DOI:10.1016/j.bbagen.2016.02.009
摘要
Transforming growth factor beta inducible early gene-1 (TIEG-1), a member of the Krüppel-like factor, was identified as a primary response gene for TGF-β. The role of TIEG-1 in skin repair has been mainly addressed in vivo on TIEG-1 null mice model and the mechanism remains unexplored. We investigated the modulation of TIEG-1 expression in normal human skin fibroblasts by either down-expressing or overexpressing the gene. We evaluated reactive oxygen species production and the cell viability of treated cells. The effect of TIEG-1 overexpression was monitored by wound healing assay and immunofluorescence staining of actin fibers organization and alpha-smooth muscle actin (α-SMA). Western blots were carried out to identify the level of expression or phosphorylation of key proteins such as cofilin, Rho GTPases, and p38 mitogen-activated protein kinase (p38 MAPK). TIEG-1 down-regulation had a deleterious effect on the cell viability. It was significantly reduced (65 ± 5%) and exposure to ultraviolet further increased this effect (47 ± 3%). By contrast, cells overexpressing TIEG-1 had a reduced reactive oxygen species production (75%) compared to control and mock-transfected cells. This overexpression also resulted in formation of actin stress fibers and increased α-SMA expression and an enhanced wound healing feature. RhoB GTPase was upregulated and phosphorylation of cofilin and p38 MAPK was observed. TIEG-1 overexpression in normal human skin fibroblasts results in improved resistance to oxidative stress, myofibroblast-like conversion that involved RhoB signaling pathway with cofilin and p38 MAPK proteins activation. This study enlightens the role of TIEG-1 role in skin biology.
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