Previous studies have confirmed that miR‐195 expression is increased in cardiac hypertrophy, and the bioinformatics website predicted by Targetscan software shows that miR‐195 can directly target CACNB1, KCNJ2 and KCND3 to regulate Cavβ1, Kir2.1 and Kv4.3 proteins expression. The purpose of this study is to confirm the role of miR‐195 in arrhythmia caused by cardiac hypertrophy. The protein levels of Cavβ1, Kir2.1 and Kv4.3 in myocardium of HF mice were decreased. After miR‐195 was overexpressed in neonatal mice cardiomyocytes, the expression of ANP, BNP and β‐MHC was up‐regulated, and miR‐195 inhibitor reversed this phenomenon. Overexpression of miR‐195 reduced the estimated cardiac function of EF% and FS% in wild‐type (WT) mice. Transmission electron microscopy showed that the ultrastructure of cardiac tissues was damaged after miR‐195 overexpression by lentivirus in mice. miR‐195 overexpression increased the likelihood of arrhythmia induction and duration of arrhythmia in WT mice. Lenti‐miR‐195 inhibitor carried by lentivirus can reverse the decreased EF% and FS%, the increased incidence of arrhythmia and prolonged duration of arrhythmia induced by TAC in mice. After miR‐195 treatment, the protein expressions of Cavβ1, Kir2.1 and Kv4.3 were decreased in mice. The results were consistent at animal and cellular levels, respectively. Luciferase assay results showed that miR‐195 may directly target CACNB1, KCNJ2 and KCND3 to regulate the expression of Cavβ1, Kir2.1 and Kv4.3 proteins. MiR‐195 is involved in arrhythmia caused by cardiac hypertrophy by inhibiting Cavβ1, Kir2.1 and Kv4.3.

中文翻译：

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通过靶向钙和钾通道，miR-195的上调有助于心脏肥大引起的心律不齐。

先前的研究已经证实，心肌肥大中miR-195表达增加，Targetscan软件预测的生物信息学网站显示，miR-195可以直接靶向CACNB1，KCNJ2和KCND3来调节Cavβ1，Kir2.1和Kv4.3蛋白的表达。这项研究的目的是确认miR-195在由心脏肥大引起的心律不齐中的作用。HF小鼠心肌中Cavβ1，Kir2.1和Kv4.3的蛋白水平降低。在新生小鼠心肌细胞中miR-195过表达后，ANP，BNP和β-MHC的表达上调，miR-195抑制剂逆转了这一现象。miR-195的过表达降低了野生型（WT）小鼠的EF％和FS％的估计心脏功能。透射电子显微镜显示，慢病毒在小鼠体内miR-195过表达后，心脏组织的超微结构受到破坏。miR-195过表达增加了WT小鼠心律不齐的诱发率和心律失常的持续时间。慢病毒携带的Lenti‐miR‐195抑制剂可以逆转由ＴＡＣ引起的小鼠EF％和FS％降低，心律不齐的发生率增加以及心律失常持续时间延长。经过miR-195处理后，小鼠中Cavβ1，Kir2.1和Kv4.3的蛋白表达降低。结果分别在动物和细胞水平上是一致的。萤光素酶检测结果表明，miR-195可能直接靶向CACNB1，KCNJ2和KCND3来调节Cavβ1，Kir2.1和Kv4.3蛋白的表达。MiR-195通过抑制Cavβ1，Kir2参与心脏肥大引起的心律失常。