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Modulation of apoptosis-related microRNAs following myocardial infarction in fat-1 transgenic mice vs wild-type mice

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机构: [1]Cardic Rehabilitation Department, Guangdong General Hospital, Guangdong Cardiovascular Institute, Guangdong Academy of Medical Sciences, Guangzhou,China [2]Intensive Care Research Team of Traditional Chinese Medicine, 2nd Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangdong ProvincialHospital of Chinese Medicine, Guangzhou, China [3]Laboratory of Experimental Animal, Guangzhou University of Chinese Medicine, Guangzhou, China [4]Intensive Care Unit of Guangdong Geriatric Institute, Guangdong General Hospital and Guangdong Academy of Medical Sciences, Guangzhou, China [5]Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China [6]Department of Cardiovascular Medicine, 2nd Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China
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关键词: fat-1 heart miRNAs myocardial infarction omega-3 polyunsaturated fatty acid

摘要:
Background microRNAs (miRNAs) post-transcriptionally regulate cardiac repair following myocardial infarction (MI). Omega-3 polyunsaturated fatty acid (-3 PUFAs) may support cardiac healing after MI, but the mechanism is unclear. MethodsResultsThe fat-1 transgenic mouse expresses a -3 fatty acid desaturase which converts -6 PUFAs to -3 PUFAs invivo. MI was induced in fat-1 transgenic (n=30) and wild-type (WT) mice (n=30) using permanent ligation. Other transgenic and WT mice underwent sham procedure (n=30 and n=30, respectively). One week after occlusion, cardiac function was measured by echocardiography and the infarct size was assessed using histology and miRNA microarray profiling. Expression of selected miRNA was confirmed using quantitative real-time PCR. One week following MI, the fat-1 transgenic myocardium had better cardiac function, a smaller fibrotic area, and fewer apoptotic cardiomyocytes than WT myocardium. Post-MI profiling showed 33 miRNAs that were significantly up-regulated, and 35 were down-regulated, in fat-1 group compared to the WT group (n=3 and n=2 mice, respectively). Among selected apoptosis-associated miRNAs, 9 miRNAs were up-regulated (miR-101a-3p, miR-128-3p,miR-133a-5p,miR-149-5p,miR-192-5p,miR-1a-3p,miR-208a-3p,miR-29c-5p,miR-30c-2-3p), and 3 were down-regulated (miR-210-3p,miR-21a-3p,miR-214-3p) in fat-1 transgenic mice compared with WT mice. Kyoto encyclopaedia of genes and genomes (KEGG) pathway analysis indicated likely roles for these miRNAs in MI. Furthermore, Bcl-2 expression was increased, and caspase-3 decreased, in infarcted fat-1 transgenic mouse hearts compared to WT hearts. Conclusions-3 PUFAs may have a protective effect on cardiomyocytes following MI through their modulation of apoptosis-related miRNAs and target genes.

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出版当年[2017]版:
大类 | 2 区 医学
小类 | 2 区 医学:研究与实验 3 区 细胞生物学
最新[2025]版:
大类 | 3 区 医学
小类 | 3 区 细胞生物学 3 区 医学:研究与实验
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出版当年[2016]版:
Q1 MEDICINE, RESEARCH & EXPERIMENTAL Q2 CELL BIOLOGY
最新[2024]版:
Q2 CELL BIOLOGY Q2 MEDICINE, RESEARCH & EXPERIMENTAL

影响因子: 最新[2024版] 最新五年平均 出版当年[2016版] 出版当年五年平均 出版前一年[2015版] 出版后一年[2017版]

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第一作者机构: [1]Cardic Rehabilitation Department, Guangdong General Hospital, Guangdong Cardiovascular Institute, Guangdong Academy of Medical Sciences, Guangzhou,China
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通讯机构: [5]Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China [6]Department of Cardiovascular Medicine, 2nd Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China [*1]Guangdong General Hospital, Guangdong Academy of Medical Sciences, 102 Zhongshan Road,Guangzhou, Guangdong, China [*2]Department of Cardiovascular Medicine, 2nd Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangdong Academy of Chinese Medical Sciences, 111 Dade Road, Guangzhou, Guangdong, China
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