Tensile strain increases expression of CCN2 and COL2A1 by activating TGF-β-Smad2/3 pathway in chondrocytic cells.
作者： Takayuki Furumatsu , Emi Matsumoto , Tomoko Kanazawa , Masataka Fujii , Zhichao Lu
DOI: 10.1016/J.JBIOMECH.2013.03.028
关键词:
摘要: Physiologic mechanical stress stimulates expression of chondrogenic genes, such as multifunctional growth factor CYR61/CTGF/NOV (CCN) 2 and alpha 1(II) collagen (COL2A1), maintains cartilage home-ostasis. In our previous studies, cyclic tensile strain (CTS) induces nuclear translocation transforming (TGF)-beta receptor-regulated Smad2/3 the master transcription Srytype HMG box (SOX) 9. However, precise mechanism stretch-mediated Smad activation remains unclear in transcriptional regulation CCN2 COL2A1. Here we hypothesized that CTS may induce TGF-beta 1 release stimulate Smad-dependent gene human chondrocytic SW1353 cells. Uni-axial (0.5 Hz, 5% strain) stimulated COL2A1 cells, induced secretion. synthesis translocalization SOX9 were by CTS. addition, increased complex formation between phosphorylated SOX9. The promoter activity was cooperatively enhanced CIS Smad3 luciferase reporter assay. Chromatin immunoprecipitation revealed interaction with enhancer. Our results suggest epigenetically via associated enhances through Smad2/3.
okayama-u.ac.jp
elsevier.com
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