Haploinsufficiency of Hand1 improves mice survival after acute myocardial infarction through preventing cardiac rupture.
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.
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. Electronic address: Lushuangshuang@zzu.edu.cn.
Shuangshuang
S
Lu
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.
Pan
P
Du
Model Animal Research Center of Nanjing University, Nanjing, China.
Congjia
C
Shan
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.
Yaohe
Y
Wang
Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Changsheng
C
Ma
Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Jianzeng
J
Dong
D000818:Animals; D017209:Apoptosis / Q000235:genetics; D051792:Basic Helix-Loop-Helix Proteins / Q000235:genetics* / Q000378:metabolism; D015153:Blotting, Western; D004452:Echocardiography; D057895:Haploinsufficiency; D006321:Heart / Q000503:physiopathology; D006341:Heart Rupture / Q000235:genetics* / Q000378:metabolism / Q000401:mortality; D006579:Heterozygote; D020778:Matrix Metalloproteinase 2 / Q000235:genetics / Q000378:metabolism; D020780:Matrix Metalloproteinase 9 / Q000235:genetics / Q000378:metabolism; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008856:Microscopy, Fluorescence; D009203:Myocardial Infarction / Q000235:genetics* / Q000378:metabolism / Q000401:mortality; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D016019:Survival Analysis; D015996:Survival Rate
D051792:Basic Helix-Loop-Helix Proteins; D020778:Matrix Metalloproteinase 2; D020780:Matrix Metalloproteinase 9; C095572:Hand1 protein, mouse
Cardiac rupture; Cardiomyocytes apoptosis; Hand1; MMP9 activity; Myocardial infarction