扩张型心肌病
收缩性
形状记忆合金*
心力衰竭
心肌病
基因剔除小鼠
心肌细胞
苏氨酸
心肌
心功能曲线
内科学
生物
内分泌学
医学
心脏病学
细胞生物学
丝氨酸
受体
磷酸化
组合数学
数学
作者
Xin Xiong,Honghui Ma,Jing Ma,Xiulong Wang,Dongxu Li,Lin Xu
标识
DOI:10.1016/j.bbrc.2022.07.106
摘要
Dilated cardiomyopathy, a type of heart muscle disease defined by the presence of left ventricular dilatation and contractile dysfunction, is an important cause of sudden cardiac death and heart failure. O-GlcNAcylation is an important post-translational modification of proteins by the addition of O-GlcNAc moieties at serine or threonine residues. Several studies have shown that proper control of O-GlcNAcylation is required for maintaining physiological function of heart by using Ogt (O-GlcNAc transferase) cardiomyocyte-specific knockout mouse models. In this study, we generated a new mouse model (αSMA-Ogt KO) in which Ogt was deleted in both cardiomyocytes and smooth muscle cells by crossing Ogt floxed mice with αSMA-Cre mice. αSMA-Cre-mediated Ogt deletion in mice led to severe postnatal lethality; the survived mice were smaller than control mice, had dilated hearts, and showed observable signs of heart failure. Moreover, the αSMA-Ogt KO heart had more apoptotic cells and fibrosis. The arteries of αSMA-Ogt KO mice exhibited significantly reduced expression of contractile genes and a trend towards arterial stiffness. In conclusion, our data emphasize the importance of OGT in maintaining normal heart function and reveal a novel role of OGT in regulating arterial contractility.
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