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Publication : Transient Receptor Potential Channel Canonical Type 3 Deficiency Antagonizes Myofibroblast Transdifferentiation In Vivo.

First Author  Xia W Year  2020
Journal  Biomed Res Int Volume  2020
Pages  1202189 PubMed ID  32219126
Mgi Jnum  J:299891 Mgi Id  MGI:6490785
Doi  10.1155/2020/1202189 Citation  Xia W, et al. (2020) Transient Receptor Potential Channel Canonical Type 3 Deficiency Antagonizes Myofibroblast Transdifferentiation In Vivo. Biomed Res Int 2020:1202189
abstractText  Objective: Myofibroblast transformation has been shown to be associated with the reactive oxygen species- (ROS-) producing enzyme NADPH oxidase (Nox4). Inhibition of transient receptor potential channel canonical type 3 (TRPC3) attenuates mitochondrial calcium handling and ROS production in the vasculature of hypertensive rats. However, it remains elusive whether TRPC3 regulates mitochondrial calcium and ROS production and participates in myofibroblast transdifferentiation during wound healing. Methods and Results: In this study, we demonstrated that activation of TRPC3 by transforming growth factor beta (TGFbeta (TGFalphaSMA). Inhibition of TRPC3 with its specific inhibitor, Pyr3, significantly decreased TGFbeta (TGFalphaSMA). Inhibition of TRPC3 with its specific inhibitor, Pyr3, significantly decreased TGFbeta (TGFbeta (TGFTrpc3(-/-) mice exhibited significantly attenuated myofibroblast transdifferentiation, as demonstrated by decreased alphaSMA). Inhibition of TRPC3 with its specific inhibitor, Pyr3, significantly decreased TGFbeta (TGFbeta (TGFTrpc3(-/-) mice exhibited significantly attenuated myofibroblast transdifferentiation, as demonstrated by decreased Trpc3(+/+) mice. In addition, Trpc3(-/-) mice exhibited significantly attenuated myofibroblast transdifferentiation, as demonstrated by decreased. Conclusions: Our data indicate that TGFbeta1-mediated activation of TRPC3 enhances mitochondrial calcium and ROS production, which promotes myofibroblast transdifferentiation and HTS formation. Inhibition of the TRPC3-mediated Nox4/pSmad2/3 pathway may be a useful strategy to limit HTS formation after injury.beta (TGF.
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