Premium
Regulation of chondrocyte proliferation through GIT1‐Rac1‐mediated ERK1/2 pathway by PDGF
Author(s) -
Xiao Jin,
Chen Xuqiong,
Xu Lipeng,
Zhang Ying,
Yin Qingshui,
Wang Fei
Publication year - 2014
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.10241
Subject(s) - rac1 , platelet derived growth factor receptor , chondrocyte , microbiology and biotechnology , downregulation and upregulation , phosphorylation , cell growth , signal transduction , aggrecan , platelet derived growth factor , growth factor , cancer research , biology , chemistry , cartilage , receptor , medicine , biochemistry , osteoarthritis , anatomy , pathology , articular cartilage , alternative medicine , gene
There are many growth factors contributing to fracture healing after bone fractures. Platelet‐derived growth factor (PDGF) released from platelets is a factor promoting cell division and proliferation, and first appears around the sites of fractures. Culture of chondrocytes in vitro are stimulated by PDGF to proliferation, its presence being upregulated in the extracellular matrix of cartilage; the main components include aggrecan and type II collagen. PDGF induces the expression of G the protein‐coupled receptor kinase interacting protein 1 (GIT1), promoting Rac1 and ERK1/2 phosphorylation. Both knocking down GIT1 expression by siRNA and blocking phosphorylation of Rac1 inhibit this induced proliferation of chondrocyte. GIT1 and Rac1 control each other, having a synergistic effect on activation of the ERK1/2 pathway. The results suggest that PDGF regulates chondrocyte proliferation through activation of ERK1/2 pathway by upregulation of GIT1 expression and Rac1 phosphorylation.