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[1]谢洪洋 闫小响 章航 范骎 陆林 沈卫峰.C1ORF54在小鼠心肌梗死后心脏修复中的作用[J].国际心血管病杂志,2019,01:26-30.
　XIE Hongyang,YAN Xiaoxiang,ZHANG Hang,et al.Effects of C1ORF54 on cardiac repair after myocardial infarction in mice[J].International Journal of Cardiovascular Disease,2019,01:26-30.
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C1ORF54在小鼠心肌梗死后心脏修复中的作用(PDF)

《国际心血管病杂志》[ISSN:1006-6977/CN:61-1281/TN]

期数:
2019年01期
页码:
26-30
栏目:
基础研究
出版日期:
2019-02-20

文章信息/Info

Title:
Effects of C1ORF54 on cardiac repair after myocardial infarction in mice
作者:
谢洪洋 闫小响 章航 范骎 陆林 沈卫峰
200025 上海交通大学医学院附属瑞金医院心脏科
Author(s):
XIE Hongyang;  YAN Xiaoxiang;  ZHANG Hang;  FAN Qin;  LU Lin;  SHEN Weifeng
Department of Cardiology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China
关键词:
1号染色体开放读码框54位基因编码蛋白;  心肌梗死;  心脏修复
Keywords:
C1ORF54;  Myocardial infarction;  Cardiac repair
分类号:
-
DOI:
10.3969/j.issn.1673-6583.2019.01.007
文献标识码:
-
摘要:
目的:探讨1号染色体开放读码框54位基因编码蛋白(C1ORF54)在小鼠心肌梗死后心脏修复中的作用及其机制。方法:选择C1ORF54基因敲除小鼠与野生型小鼠,采用结扎冠状动脉左前降支制作心肌梗死小鼠模型。21 d后以超声心动图测定各组小鼠心功能相关指标,Masson染色法观察心脏组织纤维化程度。应用免疫组织化学染色法检测心肌梗死后第3天心脏Ki-67蛋白表达变化; 应用Western blot定量测定各组小鼠p38丝裂原活化蛋白激酶/磷酸化的p38丝裂原活化蛋白激酶(p38/p-P38)、信号转导及转录激活因子3/磷酸化的信号转导及转录激活因子3(STAT3/p-STAT3)、β-连环蛋白(β-catenin)和磷酸化蛋白激酶B(p-AKT)等的表达水平。结果:心肌梗死21 d后, 尽管两组小鼠的心率相似, 但与野生型小鼠相比,C1ORF54基因敲除小鼠左室舒张末期内径[(6.04±0.14)mm对(5.41±0.17)mm]和收缩末期内径[(5.77±0.15)mm对(5.07±0.19)mm]明显增大,而射血分数明显降低[(18.75±3.03)%)对(23.12±0.70)%],P均<0.01。C1ORF54基因敲除小鼠心肌纤维化程度增高, Ki-67阳性细胞数明显减少。两组小鼠心肌p38/p-P38、STAT3/p-STAT3、β-catenin的蛋白表达水平无统计学差异,C1ORF54基因敲除小鼠p-AKT的蛋白表达水平较野生型小鼠明显降低(P<0.05)。结论:C1ORF54可能通过调控PI3K/AKT信号通路,影响心肌纤维增殖,在心肌梗死后心脏组织修复中发挥重要作用。
Abstract:
Objective:To investigate the effects and mechanisms of C1ORF54 on cardiac repair after myocardial infarction.Methods:Myocardial infarction model was established by ligating left anterior coronary artery in wild-type and C1ORF54 knockout mice. Twenty-one days later, left ventricular size and function were determined by echocardiography, and the degree of myocardial fibrosis was assessed by Masson technique. Myocardial Ki-67 expression was evaluated by immunohistochemistry at the third day after myocardial infarction. The expression of regulatory pathways including p38/p-P38, STAT3/p-STAT3, β-catenin and p-AKT was quantified by western blot.Results:Twenty-one days after myocardial infarction, despite similar heart rate, the left ventricular end-diastolic [(6.04±0.14)mm vs.(5.41±0.17)mm] and end-systolic diameters [(5.77±0.15)mm vs.(5.07±0.19)mm] were greater, while ejection fraction [(18.75±3.03)% vs.(23.12±0.70)%] was lower in C1ORF54 knockout mice than those in wild-type mice(all P<0.01).The degree of myocardial fibrosis was higher while the number of Ki-67 positive cells was lower in C1ORF54 knockout mice. Although the expression of p38/p-P38, STAT3/p-STAT3, and β-catenin was similar, the p-AKT phosphorylation of infarct myocardium was considerably reduced in C1ORF54 knockout mice(P<0.05).Conclusions:The present study suggests that C1ORF54 promotes cardiac repair after myocardial infarction through PI3K/AKT signaling pathway.

参考文献/References


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备注/Memo

备注/Memo:
基金项目:国家自然科学基金(81670457,91539117)
作者单位:200025 上海交通大学医学院附属瑞金医院心脏科
通信作者:陆林,Email:rjlulin1965@163.com
更新日期/Last Update: 2019-02-25