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1、Ischemia Impairs the Association Between Connexin 43 and M3 Subtype of Acetylcholine Muscarinic Receptor (M3- mAChR) in Ventricle MyocytesDe-Li Dong Department of Pharmacology, Harbin Medical University, Harbin, P.R.ChinaIntroduction1. Multiple subtypes of muscarinic acetylcholine receptors expresse
2、d in myocardium, including M1,M2,M3,M5-R. (Mol Pharmacol. 2001 ;59:1029-36.) 2. The M3 Receptor-mediated K+ Current (IKM3), a Gq Protein-coupled K+ Channel. (J Biol Chem.2004, 279, 21774-8) 3. Connexin 43(Cx43)-gap junction channels. (Cell 1996;84(3):381-8.) 4. Vagal nerve stimulation exerts antiarr
3、hythmogenic effects accompanied by prevention of the loss of Cx43 during acute MI.(Circulation. 2005 ;112(2):164-70.)The association between Connexin43 and M3-mAChR in ventricular myocytes.The role of M3-mAChR in cytoprotection of myocardial infarction.IntroductionResults1.Expression of M3-R and Con
4、nexin 43 in the heart.A confocal image showing the expression of connexin 43 in myocardium under control conditions and after ischemia.A confocal image showing the expression of connexin 43 (red) and M3-mAChR in a isolated myocyte.2. Connexin 43 is coimmunoprecipitated with M2/M3-R3. The effects of
5、ischemia on the expression of M-R and connexin 43. The effect of ischemia on the expression of connexin 43 in the plasma membrane. The effect of ischemia on the association between M2 or M3- mAChR and connexin 43. 4. The effect of choline pretreatment on the association between M3/M2 mAChR and conne
6、xin 43. 5. Effects of Choline on Hemodynamic Parameters during Coronary Artery Occlusion.6. Effects of choline on ischemic arrhythmias and the potential role of M3-mAChRs. 7. Effect of choline on infarct size and the potential role of M3-mAChRs. 8. Effect of choline on cardiomyocytes apoptosis and the potential role of M3-mAChRs. ConclusionsvConnexin 43 interacts with M2/M3-mAChRvIschemia specifically impairs the association between M3-mAChR and connexin 43.vCholine improves cardiac function and reduces ischemic myocardial injuries via stimulating the cardiac M3-mAChRs.
