Regulation of chondrocyte proliferation through GIT1‐Rac1‐mediated ERK1/2 pathway by PDGF. (10th February 2014)

• Record Type: Journal Article
• Authors: Xiao, Jin; Chen, Xuqiong; Xu, Lipeng; Zhang, Ying; Yin, Qingshui; Wang, Fei
• Is Part Of: Cell biology international. Volume 38:Number 6(2014)
• Page Start: 695
• Page End: 701
• Publication Date: 2014-02-10
• Subjects: Cytology -- Periodicals; Cells -- Periodicals; 571.605
• DOI: 10.1002/cbin.10241
• Languages: English
• ISSNs: 1065-6995

Abstract

<abstract abstract-type="main" xml:lang="en"> <title>Abstract</title> <sec id="cbin10241-sec-0001" sec-type="section"> <p>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.</p> </sec> </abstract>