Open AccessBone marrow mesenchymal stem cells protected post‐infarcted myocardium against arrhythmias via reversing potassium channels remodelling
Author(s) -
Cai Benzhi,
Wang Gang,
Chen Nan,
Liu Yanju,
Yin Kun,
Ning Chunping,
Li Xingda,
Yang Fan,
Wang Ning,
Wang Yang,
Pan Zhenwei,
Lu Yanjie
Publication year - 2014
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.12287
Subject(s) - transplantation , medicine , myocardial infarction , cardiology , mesenchymal stem cell , calcineurin , bone marrow , cardiac function curve , ventricular remodeling , heart failure , pathology
Bone marrow mesenchymal stem cells ( BMSC s) emerge as a promising approach for treating heart diseases. However, the effects of BMSC s‐based therapy on cardiac electrophysiology disorders after myocardial infarction were largely unclear. This study was aimed to investigate whether BMSC s transplantation prevents cardiac arrhythmias and reverses potassium channels remodelling in post‐infarcted hearts. Myocardial infarction was established in male SD rats, and BMSC s were then intramyocardially transplanted into the infarcted hearts after 3 days. Cardiac electrophysiological properties in the border zone were evaluated by western blotting and whole‐cell patch clamp technique after 2 weeks. We found that BMSC s transplantation ameliorated the increased heart weight index and the impaired LV function. The survival of infarcted rats was also improved after BMSC s transplantation. Importantly, electrical stimulation‐induced arrhythmias were less observed in BMSC s‐transplanted infarcted rats compared with rats without BMSC s treatment. Furthermore, BMSC s transplantation effectively inhibited the prolongation of action potential duration and the reduction of transient and sustained outward potassium currents in ventricular myocytes in post‐infarcted rats. Consistently, BMSC s‐transplanted infarcted hearts exhibited the increased expression of K V 4.2, K V 4.3, K V 1.5 and K V 2.1 proteins when compared to infarcted hearts. Moreover, intracellular free calcium level, calcineurin and nuclear NFAT c3 protein expression were shown to be increased in infarcted hearts, which was inhibited by BMSC s transplantation. Collectively, BMSC s transplantation prevented ventricular arrhythmias by reversing cardiac potassium channels remodelling in post‐infarcted hearts.