M3-mAChR Stimulation Exerts Anti-apoptotic Effect Via Activating the HIF-1α/HO-1/VEGF Signaling Pathway in H9c2 Rat Ventricular Cells

• DOI: 10.1097/fjc.0b013e31826c1c13
• Publication Date: 2012-08-29T09:59:19Z
• Authors: Yang Hui; Yanli Zhao; Ning Ma; Yahui Peng; Zhenwei Pan; Chaoxia Zou; Pengxia Zhang; Zhimin Du
• Keywords: Cytoprotection

The protective role of M(3)-mAChR against apoptosis has been identified previously. However, the underlying mechanisms remain unclear. This study was performed to clarify signaling pathways anti-apoptotic effect mediated by activation in cultured cardiac H9c2 cells.Both rat ventricular cells and with stable expression were used.Activation cabarchol produced on etoposide-induced cells. Forced overexpression further enhanced this effect. Application 4-diphenyl-acetoxy-N-methyl-piperidine methiodide (inhibitor M(3)-mAChR), YC-1 [inhibitor hypoxia-inducible factor 1, (HIF-1], or ZnPP heme oxygenase-1)abrogated carbacol-induced cardioprotection, respectively. Moreover, HIF-1α, HO-1, vascular endothelial growth (VEGF) after M3-mAChR, induction HO-1 VEGF reversed HIF-1α inhibitor YC-1.These findings indicated that upregulates likely through which at least partly underlies cytoprotection