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TGFβ1 induces hypertrophic change and expression of angiogenic factors in human chondrocytes
Author(s) -
Jielin Chen,
Chang Zou,
Yunfang Chen,
Weimin Zhu,
Wei Liu,
Jianghong Huang,
Qisong Liu,
Daming Wang,
Duan Li,
Jianyi Xiong,
Jiaming Cui,
Zhaofeng Jia,
Daping Wang
Publication year - 2017
Publication title -
oncotarget
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.373
H-Index - 127
ISSN - 1949-2553
DOI - 10.18632/oncotarget.20509
Subject(s) - chondrocyte , cartilage , transforming growth factor , osteoarthritis , microbiology and biotechnology , context (archaeology) , signal transduction , medicine , cancer research , biology , pathology , anatomy , paleontology , alternative medicine
The transforming growth factor β1 (TGFβ1) plays an important role in cartilage development. However, whether TGFβ1 stimulates chondrocyte proliferation and cartilage regeneration in osteoarthritis (OA) remains elusive, especially in the context of different treatment and tissue environments. In the present study, we investigated the role of TGFβ1 in human chondrocyte culture in vitro , focusing on the morphological change of chondrocytes and the expression of angiogenic factors upon TGFβ1 stimulation. We found increased expression of biomarkers indicating chondrocyte hypertrophy and the chondrocytes aggregated to form networks when they were treated with TGFβ1. DNA microarray analysis revealed significantly increased expression of genes related to blood vessel formation in TGFβ1 treatment group compared to control group. Matrigel assay further demonstrated that chondrocytes had the potential to form network-like structure. These results suggested that TGFβ1 induces the hypertrophic change of chondrocytes culture in vitro and induce expression of angiogenic biomarkers. Therefore, application of TGFβ1 for chondrocyte culture in practice should be considered prudentially and targeting TGFβ1 or relevant receptors to block the signaling pathway might be a strategy to prevent or alleviate progression of osteoarthritis.

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