The effect of type II collagen on MSC osteogenic differentiation and bone defect repair

被引:120
作者
Chiu, Li-Hsuan [1 ]
Lai, Wen-Fu T. [1 ,2 ,3 ]
Chang, Shwu-Fen [1 ]
Wong, Chin-Chean [4 ]
Fan, Cheng-Yu [5 ]
Fang, Chia-Lang [6 ]
Tsai, Yu-Hui [1 ,3 ]
机构
[1] Taipei Med Univ, Grad Inst Med Sci, Taipei 11031, Taiwan
[2] Taipei Med Univ, Grad Inst Clin Med, Taipei 11031, Taiwan
[3] Taipei Med Univ, Ctr Nano Biomed Res, Taipei 11031, Taiwan
[4] Taipei Med Univ, Wanfang Hosp, Dept Orthopaed Surg, Taipei 11031, Taiwan
[5] Taipei Med Univ Hosp, Dept Orthopaed Surg, Taipei 11031, Taiwan
[6] Taipei Med Univ, Coll Med, Sch Med, Dept Pathol, Taipei 11031, Taiwan
关键词
Mesenchymal stem cell; Type II collagen; Osteogenesis; Cell adhesion; Integrin signaling; Bone healing; MESENCHYMAL STEM-CELLS; FOCAL ADHESION KINASE; TRANSGENIC MICE; CHONDROGENIC DIFFERENTIATION; SIGNAL-TRANSDUCTION; GENE; EXPRESSION; STIMULATION; CARTILAGE; PATHWAYS;
D O I
10.1016/j.biomaterials.2013.12.005
中图分类号
R318 [生物医学工程];
学科分类号
0831 ;
摘要
The function of type II collagen in cartilage is well documented and its importance for long bone development has been implicated. However, the involvement of type II collagen in bone marrow derived mesenchymal stem cell (BMSC) osteogenesis has not been well investigated. This study elucidated the pivotal role of type II collagen in BMSC osteogenesis and its potential application to bone healing. Type II collagen-coated surface was found to accelerate calcium deposition, and the interaction of osteogenic medium-induced BMSCs with type II collagen-coated surface was mainly mediated through integrin alpha 2 beta 1. Exogenous type II collagen directly activated FAK-JNK signaling and resulted in the phosphorylation of RUNX2. In a segmental defect model in rats, type II collagen-HA/TCP-implanted rats showed significant callus formation at the reunion site, and a higher SFI (sciatic function index) scoring as comparing to other groups were also observed at 7, 14, and 21 day post-surgery. Collectively, type II collagen serves as a better modulator during early osteogenic differentiation of BMSCs by facilitating RUNX2 activation through integrin alpha 2 beta 1-FAK-JNK signaling axis, and enhance bone defect repair through an endochondral ossification-like process. These results advance our understanding about the cartilaginous ECM-BMSC interaction, and provide perspective for bone defect repair strategies. (C) 2013 Elsevier Ltd. All rights reserved.
引用
收藏
页码:2680 / 2691
页数:12
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