W Su1, P Wang, H Chen, H Li. 1. Department of Cardiology, Beijing Friendship Hospital, Capital Medical University, No. 95, Yongan Road, Xicheng District, Beijing, 100050, People's Republic of China.
Abstract
INTRODUCTION: Relaxin is a pleiotropic hormone owing endogenous antifibrosis effect on numerous organs. We demonstrated relaxin's inhibitive effect on cardiac fibrosis previously. OBJECTIVE: The aim of this study was to investigate the role of protein kinase C (PKC) β2 in relaxin's action under high glucose conditions. METHODS AND RESULTS: Cardiac fibroblasts (CFs) were isolated, exposed to high glucose and incubated with recombinant human relaxin (rhRLX). Western blot analysis revealed a relaxin-mediated decrease in total expression and translocation of PKCβ2, showing downregulation of PKCβ2 is involved in relaxin's action. Blocking PKCβ2 pathway with ruboxistaurin accelerated rhRLX-mediated inhibition in both proliferation of CFs and deposition of collagen. CONCLUSION: In conclusion, relaxin can inhibit high glucose-associated cardiac fibrosis partly through PKCβ2 pathway. Further work should be done to fully understand intracellular mechanisms of relaxin's action to accelerate its clinical use.
INTRODUCTION: Relaxin is a pleiotropic hormone owing endogenous antifibrosis effect on numerous organs. We demonstrated relaxin's inhibitive effect on cardiac fibrosis previously. OBJECTIVE: The aim of this study was to investigate the role of protein kinase C (PKC) β2 in relaxin's action under high glucose conditions. METHODS AND RESULTS: Cardiac fibroblasts (CFs) were isolated, exposed to high glucose and incubated with recombinant human relaxin (rhRLX). Western blot analysis revealed a relaxin-mediated decrease in total expression and translocation of PKCβ2, showing downregulation of PKCβ2 is involved in relaxin's action. Blocking PKCβ2 pathway with ruboxistaurin accelerated rhRLX-mediated inhibition in both proliferation of CFs and deposition of collagen. CONCLUSION: In conclusion, relaxin can inhibit high glucose-associated cardiac fibrosis partly through PKCβ2 pathway. Further work should be done to fully understand intracellular mechanisms of relaxin's action to accelerate its clinical use.
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