The role of ERK and JNK signaling in connective tissue growth factor induced extracellular matrix protein production and scar formation
The role of ERK and JNK signaling in connective tissue growth factor induced extracellular matrix protein production and scar formation
复制标题
ERK和JNK信号在结缔组织生长因子诱导细胞外基质蛋白产生和疤痕形成中的作用
DOI：
10.1007/s00403-013-1334-9
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发表时间：
2013-07-01
影响因子：
3
通讯作者：
Hu, Dahai
中科院分区：
文献类型：
--
作者：
Hu, Xiaolong;Wang, Hongtao;Hu, Dahai
CCN2 plays an important role in the pathogenesis of hypertrophic scars (HTSs). Although CCN2 is involved in many fibroproliferative events, the CCN2 induction signaling pathway in HTSs is yet to be elucidated. Here, we first investigated the effect of the mitogen-activated protein kinases (MAPKs) on CCN2-induced α-smooth muscle actin (α-SMA) and collagen I expression in human HTS fibroblasts (HTSFs). Then, we established HTSs in a rabbit ear model and determined the effect of MAPKs on the pathogenesis of HTSs. MAPK pathways were activated by CCN2 in HTSFs. Extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) inhibitors significantly inhibited CCN2-induced expression of α-SMA and collagen I in HTSFs. In the rabbit ear model of the HTS, JNK and ERK inhibitors significantly improved the architecture of the rabbit ear scar and reduced scar formation on the rabbit ear. Our results indicate that ERK and JNK mediate collagen I expression and scarring of the rabbit ear, and may be considered for specific drug therapy targets for HTSs.
