Hand1单倍剂量不足通过防止心脏破裂提高急性心肌梗死后小鼠的存活率。
Haploinsufficiency of Hand1 improves mice survival after acute myocardial infarction through preventing cardiac rupture.
作者信息
Lu Shuangshuang, Du Pan, Shan Congjia, Wang Yaohe, Ma Changsheng, Dong Jianzeng
机构信息
National Centre for International Research in Cell and Gene Therapy, School of Basic Medical Science, The Academy of Medical Science of Zhengzhou University, Zhengzhou, China; Model Animal Research Center of Nanjing University, Nanjing, China.
National Centre for International Research in Cell and Gene Therapy, School of Basic Medical Science, The Academy of Medical Science of Zhengzhou University, Zhengzhou, China.
出版信息
Biochem Biophys Res Commun. 2016 Sep 30;478(4):1726-31. doi: 10.1016/j.bbrc.2016.09.012. Epub 2016 Sep 4.
Previous studies have demonstrated a significantly lower level of Hand1 in ischemic cardiomyopathy than in normal heart tissue. The role of decreased Hand1 in myocardial infarction remains unclear. This study was designed to investigate the effects of haploinsufficiency of Hand1 on mouse heart after myocardial infarction. 8-10 weeks old male heterozygous Hand1-deficient (Hand1(+/-)) mice and wild-type littermates (control) were subjected to sham operation or ligation of the left anterior descending coronary artery to induce acute myocardial infarction (AMI). Hand1(+/-) mice have low incidence of left ventricular free wall rupture in the first week after operation than control mice. Then we found lower MMP9 activity and less cardiomyocytes apoptosis in Hand1(+/-) than in control mice. All of these contribute to the protection role of haploinsufficiency of Hand1 after AMI.
先前的研究表明，与正常心脏组织相比，缺血性心肌病中Hand1的水平显著降低。Hand1水平降低在心肌梗死中的作用仍不清楚。本研究旨在探讨Hand1单倍剂量不足对小鼠心肌梗死后心脏的影响。将8-10周龄的雄性杂合Hand1缺陷（Hand1(+/-)）小鼠和野生型同窝小鼠（对照）进行假手术或结扎左冠状动脉前降支以诱导急性心肌梗死（AMI）。与对照小鼠相比，Hand1(+/-)小鼠术后第一周左心室游离壁破裂的发生率较低。然后我们发现，与对照小鼠相比，Hand1(+/-)小鼠的MMP9活性较低，心肌细胞凋亡较少。所有这些都有助于Hand1单倍剂量不足在AMI后发挥保护作用。
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