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MicroRNA-22 Downregulation by Atorvastatin in a Mouse Model of Cardiac Hypertrophy: a new Mechanism for Antihypertrophic Intervention
Author(s) -
Yingfeng Tu,
Lin Wan,
Lihong Bu,
Dongliang Zhao,
Dandan Dong,
Tao Huang,
Zhen Cheng,
Baozhong Shen
Publication year - 2013
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000350117
Subject(s) - downregulation and upregulation , pten , tensin , atorvastatin , angiotensin ii , endocrinology , microrna , medicine , muscle hypertrophy , gene knockdown , biology , stimulation , microbiology and biotechnology , signal transduction , pi3k/akt/mtor pathway , cell culture , blood pressure , biochemistry , genetics , gene
Growing evidence shows that microRNAs (miRNAs) are involved in various cardiac processes including cardiac hypertrophy. However, the modulation of miRNA by pharmacological intervention in cardiomyocyte hypertrophy has not been disclosed yet. methods: We constructed neonatal rat cardiomyocyte hypertrophy induced by angiotensin II stimulation and subjected to cardiomyocyte immunochemistry, qRT-PCR and immunoblotting analysis. In addition, we constructed the mouse cardiac hypertrophy using angomir-22 stimulation and demonstrated the potential antihypertrophic mechnism of atorvastatin.

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