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ClC-3 chloride channel is involved in isoprenaline-induced cardiac hypertrophy
- Li, Chunmei, Huang, Dan, Tang, Jing, Chen, Mengqing, Lu, Qun, Li, He, Zhang, Mengzhen, Xu, Bin, Mao, Jianwen
- Gene 2018 v.642 pp. 335-342
- Dependovirus, beta adrenergic receptors, cardiomyocytes, gene expression, hypertrophy, isoprenaline, messenger RNA, mice, natriuretic peptides, propranolol
- Isoprenaline, an activator of β-adrenergic receptor, has been found to induce cardiac hypertrophy in vivo and in vitro, but the exact mechanism is still unclear. ClC-3 is a member of the chloride channel family and is highly expressed in mammalian myocardium. In the present study, the role of ClC-3 in isopronaline-induced cardiac hypertrophy was investigated. We found that ClC-3 expression was reduced in isoprenaline-induced hypertrophic H9c2 cells, primary rat neonatal cardiomyocytes and myocardium of C57/BL/6 mice, and this reduction was prevented by the pretreatment of propranolol. Adeno-associated virus 9 (AAV9)-mediated ClC-3 expression in myocardium decreased heart mass index, thinned interventricular septum and left ventricular wall and lowered the mRNA expression of natriuretic peptide type A (ANF) and β-myosin heavy chain (β-MHC). Our results showed that ClC-3 played an important role in β-adrenergic cardiac hypertrophy which could be associated with ANF and β-MHC, and all these findings suggested that ClC-3 may be a novel therapeutic target for the prevention or treatment of myocardiac hypertrophy.