MicroRNA‐101b attenuates cardiomyocyte hypertrophy by inhibiting protein kinase C epsilon signaling. Issue 1 (19th December 2016)

• Record Type: Journal Article
• Authors: Lee, Jong Sub; Yang, Dong Kwon; Park, Jei Hyoung; Kim, Jin Ock; Park, Woo Jin; Cho, Chunghee; Kim, Do Han
• Is Part Of: FEBS letters. Volume 591:Issue 1(2017)
• Page Start: 16
• Page End: 27
• Publication Date: 2016-12-19
• Subjects: cardiomyocytes -- miR‐101b -- microRNA -- myocardial hypertrophy -- protein kinase C -- systems biology; Biochemistry -- Periodicals; Biophysics -- Periodicals; Molecular biology -- Periodicals; Biochimie -- Périodiques; Biochemistry; Biophysics; Molecular biology; Periodicals; 572.05
• DOI: 10.1002/1873-3468.12508
• Languages: English
• ISSNs: 0014-5793

Abstract

Abstract : Previously, a surgical regression model identified microRNA‐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 (PKCε) as the major target of miR‐101b . Our results from qRT‐PCR, western blot, and luciferase reporter assays confirm that PKCε is a direct target of miR‐101b . In addition, we found that effectors downstream of PKCε (p‐AKT, p‐ERK1/2, p‐NFAT, and p‐GSK3β) are also affected by miR‐101b . Our study reveals a novel inhibitory mechanism for miR‐101b as a negative regulator of cardiac hypertrophy. Abstract :