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Focal adhesion kinase promotes BMP2‐induced osteogenic differentiation of human urinary stem cells via AMPK and Wnt signaling pathways
Author(s) -
Sun Xingwei,
Zheng Weiwei,
Qian Chen,
Wu Qin,
Hao Yuefeng,
Lu Guohai
Publication year - 2020
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29374
Subject(s) - bone morphogenetic protein 2 , microbiology and biotechnology , wnt signaling pathway , osteopontin , chemistry , focal adhesion , runx2 , ampk , osteocalcin , cellular differentiation , signal transduction , stem cell , protein kinase a , alkaline phosphatase , kinase , osteoblast , biology , endocrinology , in vitro , biochemistry , gene , enzyme
Human urine‐derived stem cells (hUSCs) serve as favorable candidates for bone transplants due to their efficient proliferative and multipotent differentiation abilities, as well as the capacity to secrete a variety of vasoactive agents to facilitate tissue engineering. The present study aimed to explore the role of focal adhesion kinase (FAK) in bone morphogenetic protein 2 (BMP2)‐induced osteogenic differentiation of hUSCs and to investigate the underlying mechanism. The degree of osteogenic differentiation and the correlated signals, following BMP2 overexpression and siRNA‐mediated silencing of FAK, were determined in vitro. Moreover, hUSCs induced bone formation in a rat model with cranial defects, in vivo. Our findings revealed that alkaline phosphatase production, calcium deposits, osteocalcin and osteopontin expression, and bone formation were upregulated in vitro and in vivo following BMP2‐induced osteogenic differentiation, and AMPK and Wnt signaling pathway activation by FAK could effectively regulate BMP2‐enhanced osteogenic differentiation of hUSCs. Taken together, these findings indicated that FAK could mediate BMP2‐enhanced osteogenic differentiation of hUSCs through activating adenosine 5’‐monophosphate‐activated protein kinase and Wnt signaling pathways.