Atorvastatin prevents Angiotensin II induced myocardial hypertrophy in vitro via CCAAT/enhancer-binding protein β.
Previous evidences suggested that atorvastatin not only reduced blood lipids but also reduced myocardial hypertrophy and remodeling. And it was reported that C/EBPβ (CCAAT/enhancer-binding protein β) played a pivotal role both in the physiologic and pathological cardiac hypertrophy. However, it has not been reported before whether this signaling pathway of C/EBPβ participates in protective effect of atorvastatin for hypertrophy cardiomyocytes. In present study, We found that overexpression of C/EBPβ significantly abrogated the effect of atorvastatin on increasing Bcl-2/Bax and PGC-1α while the early and late apoptosis rate increased and mitochondrial membrane potential (MMP) was reduced. In conclusion, we further identified the protective effect of atorvastatin on hypertrophic cardiomyocytes induced by Angiotensin II by rescuing the MMP and inhibiting apoptosis, which might be at least partly attributed to down-regulation of C/EBPβ. And C/EBPβ might be a new target to rescue mitochondrion function and apoptosis in pathological cardiac hypertrophy.
Department of Cardiology, The First Hospital of China Medical University, Shenyang, 110001, People's Republic of China. Electronic address: chenyintao1990@126.com.
Yintao
Y
Chen
Department of Cardiology, The First Hospital of China Medical University, Shenyang, 110001, People's Republic of China. Electronic address: yidasasa@foxmail.com.
Shasha
S
Yu
Department of Cardiology, The First Hospital of China Medical University, Shenyang, 110001, People's Republic of China. Electronic address: naijinzhang1989@126.com.
Naijin
N
Zhang
Department of Cardiology, The First Hospital of China Medical University, Shenyang, 110001, People's Republic of China. Electronic address: wxy13196303669@163.com.
Yuan
Y
Li
Department of Cardiology, The First Hospital of China Medical University, Shenyang, 110001, People's Republic of China. Electronic address: 13654004558@126.com.
Shuang
S
Chen
Department of Cardiology, The First Hospital of China Medical University, Shenyang, 110001, People's Republic of China. Electronic address: chang.ye@stu.xjtu.edu.cn.
Ye
Y
Chang
Department of Cardiology, The First Hospital of China Medical University, Shenyang, 110001, People's Republic of China. Electronic address: gzhsun66@163.com.
Guozhe
G
Sun
Department of Cardiology, The First Hospital of China Medical University, Shenyang, 110001, People's Republic of China. Electronic address: yxsun@cmu.edu.cn.
Yingxian
Y
Sun
D000804:Angiotensin II / Q000494:pharmacology*; D057911:Angiotensin Receptor Antagonists / Q000494:pharmacology*; D000818:Animals; D000924:Anticholesteremic Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects / Q000235:genetics; D000069059:Atorvastatin / Q000494:pharmacology*; D022782:CCAAT-Enhancer-Binding Protein-beta / Q000235:genetics* / Q000378:metabolism; D002460:Cell Line; D005786:Gene Expression Regulation; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha / Q000235:genetics / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000378:metabolism; D051381:Rats; D015398:Signal Transduction; D051028:bcl-2-Associated X Protein / Q000235:genetics / Q000378:metabolism
D057911:Angiotensin Receptor Antagonists; D000924:Anticholesteremic Agents; C494828:Bax protein, rat; C000617196:Bcl2 protein, rat; D022782:CCAAT-Enhancer-Binding Protein-beta; C545014:Cebpb protein, rat; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; C501429:Ppargc1a protein, rat; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D000804:Angiotensin II; D000069059:Atorvastatin
Apoptosis; Atorvastatin; C/EBPβ; Myocardial hypertrophy; PGC-1α