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BMP9 promotes osteogenic differentiation of SMSCs by activating the JNK/Smad2/3 signaling pathway
Author(s) -
Zheng Weiwei,
Chen Qian,
Zhang Yu,
Xia Rui,
Gu Xueping,
Hao Yuefeng,
Yu Zepeng,
Sun Xingwei,
Hu Dan
Publication year - 2020
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.29519
Subject(s) - osteopontin , osteocalcin , microbiology and biotechnology , in vivo , mesenchymal stem cell , p38 mitogen activated protein kinases , in vitro , alkaline phosphatase , signal transduction , chemistry , kinase , biology , protein kinase a , immunology , biochemistry , enzyme
Synovial mesenchymal stem cells (SMSCs) with high proliferation and multi differentiation ability, and low immunogenicity have attracted research attention for their potential application in tissue engineering. Once their ability of osteogenesis is strengthened, it will be of practical value to apply the SMSCs in the field of bone regeneration. The current study aimed to investigate the osteogenic characteristics of SMSCs induced by bone morphogenetic protein 9 (BMP9) both in vitro and in vivo and to elucidate the mechanism underlying these characteristics. Specifically, different BMPs were assessed to determine the protein that would be the most favorable for stimulating osteogenic differentiation of SMSCs following their separation. The BMP9‐enhanced osteogenesis of SMSCs was fully investigated in vitro and in vivo, and the c‐Jun N‐terminal kinase (JNK)/Smad2/3 signaling pathway stimulated by BMP9 was further explored. Our data suggested that BMP9 could significantly promote gene and protein expression of runt‐related transcription factor 2, alkaline phosphatase, osteopontin, and osteocalcin, and SP600125, a JNK‐specific inhibitor, could effectively decrease this tendency. Similar results were also confirmed in rats with cranial defects. In conclusion, our study indicated that BMP9 promotes bone formation both in vitro and in vivo possibly by activating the JNK/Smad2/3 signaling pathway.