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Micro RNA ‐101b attenuates cardiomyocyte hypertrophy by inhibiting protein kinase C epsilon signaling
Author(s) -
Lee Jong Sub,
Yang Dong Kwon,
Park Jei Hyoung,
Kim Jin Ock,
Park Woo Jin,
Cho Chunghee,
Kim Do Han
Publication year - 2017
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.12508
Subject(s) - nfat , muscle hypertrophy , western blot , protein kinase c , protein kinase b , microrna , myocyte , signal transduction , kinase , microbiology and biotechnology , medicine , downregulation and upregulation , endocrinology , biology , gene , transcription factor , biochemistry
Previously, a surgical regression model identified micro RNA ‐101b ( miR‐101b ) as a potential inhibitor of cardiac hypertrophy. Here, we investigated the antihypertrophic mechanism of miR‐101b using neonatal rat ventricular myocytes. miR‐101b markedly suppressed agonist‐induced cardiac hypertrophy as shown by cell size and fetal gene expression. By systems biology approaches, we identified protein kinase C epsilon ( PKC ε) as the major target of miR‐101b . Our results from qRT ‐ PCR , western blot, and luciferase reporter assays confirm that PKC ε is a direct target of miR‐101b . In addition, we found that effectors downstream of PKC ε (p‐ AKT , p‐ ERK 1/2, p‐ NFAT , and p‐ GSK 3β) are also affected by miR‐101b . Our study reveals a novel inhibitory mechanism for miR‐101b as a negative regulator of cardiac hypertrophy.