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Platelet-rich plasma promotes the regeneration of cartilage engineered by mesenchymal stem cells and collagen hydrogel via the TGF-β/SMAD signaling pathway
Authors:Depeng Fang  Pan Jin  Quanxin Huang  Yuan Yang  Jinmin Zhao  Li Zheng
Institution:1. Guangxi Engineering Center in Biomedical Material for Tissue and Organ Regeneration, Life Sciences Institute, Guangxi Medical University, Nanning, People's Republic of China;2. Guangxi Engineering Center in Biomedical Material for Tissue and Organ Regeneration, Life Sciences Institute, Guangxi Medical University, Nanning, People's Republic of China

Guangxi Collaborative Innovation Center for Biomedicine, Life Sciences Institute, Guangxi Medical University, Nanning, People's Republic of China

Guangxi Key Laboratory of Regenerative Medicine, Life Sciences Institute, Guangxi Medical University, Nanning, People's Republic of China

Fang and Jin have contributed equally to this study.;3. Guangxi Engineering Center in Biomedical Material for Tissue and Organ Regeneration, Life Sciences Institute, Guangxi Medical University, Nanning, People's Republic of China

Guangxi Collaborative Innovation Center for Biomedicine, Life Sciences Institute, Guangxi Medical University, Nanning, People's Republic of China

Guangxi Key Laboratory of Regenerative Medicine, Life Sciences Institute, Guangxi Medical University, Nanning, People's Republic of China

Abstract:The tissue engineering technique using mesenchymal stem cells (MSCs) and scaffolds is promising. Transforming growth factor-β1 (TGF-β1) is generally accepted as an chondrogenic agent, but immunorejection and unexpected side effects, such as tumorigenesis and heterogeneity, limit its clinical application. Autogenous platelet-rich plasma (PRP), marked by low immunogenicity, easy accessibility, and low-cost, may be favorable for cartilage regeneration. In our study, the effect of PRP on engineered cartilage constructed by MSCs and collagen hydrogel in vitro and in vivo was investigated and compared with TGF-β1. The results showed that PRP promoted cell proliferation and gene and protein expressions of chondrogenic markers via the TGF-β/SMAD signaling pathway. Meanwhile, it suppressed the expression of collagen type I, a marker of fibrocartilage. Furthermore, PRP accelerated cartilage regeneration on defects with engineered cartilage, advantageous over TGF-β1, as evaluated by histological analysis and immunohistochemical staining. Our work demonstrates that autogenous PRP may substitute TGF-β1 as a potent and reliable chondrogenic inducer for therapy of cartilage defect.
Keywords:autogenous  cartilage defect  collagen  mesenchymal stem cells  platelet-rich plasma
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