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• W3102162539 abstract "Relative resistance to apoptosis and the ability to proliferate and produce a collagen-rich scar determine the critical role of cardiac fibroblasts in wound healing and tissue remodeling following myocardial injury. Identification of cardiac fibroblast-specific factors and mechanisms underlying these aspects of cardiac fibroblast function is therefore of considerable scientific and clinical interest. In the present study, gene knockdown and over-expression approaches, and promoter binding assays, showed that DDR2, a mesenchymal cell-specific collagen receptor tyrosine kinase localized predominantly in fibroblasts in the heart, acts via ERK1/2 MAPK-activated SRF transcription factor to enhance the expression of anti-apoptotic cIAP2 in cardiac fibroblasts, conferring resistance against oxidative injury. Further, DDR2 was found to act via ERK1/2 MAPK-activated SRF to transcriptionally up-regulate Skp2 that in turn facilitated post-translational degradation of p27, the cyclin-dependent kinase inhibitor that causes cell cycle arrest, to promote G1-S transition, as evidenced by Rb phosphorylation, increased PCNA levels and flow cytometry. DDR2-dependent ERK1/2 MAPK activation also suppressed FoxO3a-mediated transcriptional induction of p27. Notably, DDR2 levels positively correlated with SRF, cIAP2 and PCNA levels in cardiac fibroblasts from Spontaneously Hypertensive Rats. To conclude, DDR2-mediated ERK1/2 MAPK activation facilitates coordinated regulation of cell survival and cell cycle progression in cardiac fibroblasts via SRF." @default.
• W3102162539 created "2020-11-23" @default.
• W3102162539 creator A5007467292 @default.
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• W3102162539 date "2019-11-27" @default.
• W3102162539 modified "2023-09-27" @default.
• W3102162539 title "Identification of a common regulatory pathway that determines cell survival and cell cycle progression in cardiac fibroblasts" @default.
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