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p38 MAPK mediated in compressive stress‐induced chondrogenesis of rat bone marrow MSCs in 3D alginate scaffolds
Author(s) -
Li Juan,
Zhao Zhihe,
Yang Jingyuan,
Liu Jun,
Wang Jun,
Li Xiaoyu,
Liu Yurong
Publication year - 2009
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.21890
Subject(s) - chondrogenesis , microbiology and biotechnology , mesenchymal stem cell , chondrocyte , aggrecan , sox9 , chemistry , runx2 , cartilage , mapk/erk pathway , p38 mitogen activated protein kinases , signal transduction , in vitro , gene expression , osteoarthritis , biology , anatomy , medicine , biochemistry , osteoblast , gene , pathology , articular cartilage , alternative medicine
Mesenchymal stem cells (MSCs) are well known to have the capability to form bone and cartilage, and chondrogenesis derived from MSCs is reported to be affected by mechanical stimuli. This research was aimed to study the effects of cyclic compressive stress on the chondrogenic differentiation of rat bone marrow‐derived MSCs (BMSCs) which were encapsulated in alginate scaffolds and cultured with or without chondrogenic medium, and to investigate the role of p38 MAPK phospho‐relay cascade in this process. The results show that the gene expression of chondrocyte‐specific markers of Col2α1, aggrecan, Sox9, Runx2, and Ihh was upregulated by dynamic compressive stress introduced at the 8th day of chondrogenic differentiation in vitro. The p38 MAPK was activated by chondrogenic cytokines in a slow and lagged way, but activated by cyclic compressive stimulation in a rapid and transient manner. And inhibition of p38 activity with SB203580 suppressed gene expression of chondrocyte‐specific genes stimulated by chondrogenic medium and (or) cyclic compressive stress. These findings suggest that p38 MAPK signal acts as an essential mediator in the mechano‐biochemical transduction and subsequent transcriptional regulation in the process of chondrogenesis. J. Cell. Physiol. 221: 609–617, 2009. © 2009 Wiley‐Liss, Inc.