TGFβ1 induces hypertrophic change and expression of angiogenic factors in human chondrocytes
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Jie-Lin Chen1,2,*, Chang Zou3,4,*, Yunfang Chen1,5, Weimin Zhu1,2, Wei Liu1,2, Jianghong Huang1,2, Qisong Liu1,2, Daming Wang1,2, Li Duan1,2, Jianyi Xiong1,2, Jiaming Cui1,2, Zhaofeng Jia1,2 and Daping Wang1,2
1Shenzhen Key Laboratory of Tissue Engineering, Shenzhen Second People’s Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen 518035, Guangdong Province, China
2Shenzhen Centre for Sports Medicine and Engineering Technology, Shenzhen 518035, Guangdong Province, China
3Shenzhen Public Service Platform for Cancer Precision Medicine and Molecular Diagnosis, Shenzhen 518020, China
4Clinical Medical Research Center, The Second Clinical Medical College, Shenzhen People’s Hospital, Jinan University, Shenzhen, 518020 China
5The Eighth Affiliated Hospital, Sun Yat-sen University, Shenzhen 518035, Guangdong Province, China
*These authors have contributed equally to this work
Daping Wang, email: email@example.com
Keywords: TGFβ1, chondrocyte, hypertrophy, angiogenesis, DNA microarray
Received: March 29, 2017 Accepted: August 04, 2017 Published: August 24, 2017
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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