Insulin-like growth factor-1 boosts the developing process of condylar hyperplasia by stimulating chondrocytes proliferation

被引：64

作者：

Chen, Y. ^{[1
,2
]}

Ke, J. ^{[1
,2
]}

Long, X. ^{[1
]}

Meng, Q. ^{[1
]}

Deng, M. ^{[1
]}

Fang, W. ^{[1
]}

Li, J. ^{[1
]}

Cai, H. ^{[1
]}

Chen, S. ^{[1
]}

机构：

[1] Wuhan Univ, Hubei Stomatol Hosp, Dept Oral & Maxillofacial Surg, Sch Stomatol, Wuhan, Hubei Province, Peoples R China

[2] Wuhan Univ, Sch Stomatol, Lab Oral Biomed, Wuhan, Hubei Province, Peoples R China

来源：

OSTEOARTHRITIS AND CARTILAGE | 2012年 / 20卷 / 04期

基金：

美国国家科学基金会;

关键词：

Insulin-like growth factor-1(IGF-1); Temporomandibular joint (TMJ); Condylar hyperplasia(CH); Cellular proliferation; Chondrocyte; SIGNALING PATHWAYS; KAPPA-B; CHONDROGENESIS; EXPRESSION; CARTILAGE; FIBROBLASTS; MANAGEMENT; CULTURE; KINASE; CELLS;

D O I：

10.1016/j.joca.2011.12.013

中图分类号：

R826.8 [整形外科学]; R782.2 [口腔颌面部整形外科学]; R726.2 [小儿整形外科学]; R62 [整形外科学（修复外科学）];

学科分类号：

100224 [整形外科学];

摘要：

Objective: The etiology of Condylar hyperplasia (CH) of human temporomandibular joint (TMJ) remains largely unknown. Our previous study has demonstrated that enriched insulin-like growth factor-1(IGF-1) was expressed in the proliferation and hypertrophic layers of CH cartilage. Accordingly, this study was aimed to investigate whether IGF-1 regulates CH chondrocytes proliferation in condylar cartilage overgrowth and explore the molecular mechanism of IGF-1 involved in. Methods: Chondrocytes were isolated from 6 CH and 3 normal cartilage (NC) specimens and cultured in alginate beads or monolayer, treated with IGF-1 or specific inhibitors such as 7-[trans-3-[(azetidin-1-yl)-methyl]cyclobutyl]-5-(3-benzyloxyphenyl)7H-pyrrolo[2,3-d]pyrimidin-4-amine (NVP-AEW541). U0126, and LY294002. Thereafter, cellular proliferation capacity was evaluated by Cell Viability Analyzer (alginate beads culture) or 3(4,5-dimethylthiazo(-2-yl)-2,5-diphenyltetrazolium bromide (MTT) (monolayer culture). Gene expression levels of IGF-1, IGF-1 receptor (IGF-1R), collagen type II, type X and those genes associated with proliferation were evaluated by realtime PCR. Protein levels of IGF-1 and IGF-1R synthesized by CH chondrocytes were accessed by enzyme-linked immunosorbent assay (ELISA) and western blotting. Results: CH chondrocytes enhanced cellular proliferation capacity and expressed significantly higher levels of messenger RNA (mRNA) and protein expressions of IGF-1 and IGF-1R, a; compared with NC chondrocytes. Furthermore, enriched IGF-1 enhanced CH chondrocytes proliferation, up-regulated the expressions of specific genes associated with cellular proliferation and elevated the gene expression of collagen type II A1 (COL2A1). Besides, IGF-1-mediated CH chondrocytes proliferation mainly depended on the mitogen-activated protein kinase (MAPK)-ERK pathway. Conclusions: IGF-1 promotes human TMJ cartilage overgrowth in the developing process of CH by enhancing chondrocytes proliferation via MAPK-ERK pathway. (C) 2012 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.

引用

页码：279 / 287

页数：9

共 39 条

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Enhanced Chondrocyte Proliferation and Mesenchymal Stromal Cells Chondrogenesis in Coculture Pellets Mediate Improved Cartilage Formation [J].