Effect of atorvastatin on cardiomyocyte hypertrophy through suppressing MURC induced by volume overload and cyclic stretch.
Angiotensin II
/ metabolism
Animals
Anticholesteremic Agents
/ pharmacology
Arteriovenous Shunt, Surgical
/ adverse effects
Atorvastatin
/ pharmacology
Cardiomegaly
/ drug therapy
Extracellular Signal-Regulated MAP Kinases
/ metabolism
Gene Expression Regulation
/ drug effects
Male
Muscle Proteins
/ genetics
Myocytes, Cardiac
/ drug effects
Rats
Rats, Wistar
Signal Transduction
Stress, Mechanical
MURC
atorvastatin
cyclic stretch
volume overload
Journal
Journal of cellular and molecular medicine
ISSN: 1582-4934
Titre abrégé: J Cell Mol Med
Pays: England
ID NLM: 101083777
Informations de publication
Date de publication:
02 2019
02 2019
Historique:
received:
13
09
2018
revised:
24
10
2018
accepted:
31
10
2018
pubmed:
5
12
2018
medline:
1
7
2020
entrez:
5
12
2018
Statut:
ppublish
Résumé
MURC (muscle-restricted coiled-coil protein) is a hypertrophy-related gene. Hypertrophy can be induced by mechanical stress. The purpose of this research was to investigate the hypothesis that MURC mediates hypertrophy in cardiomyocytes under mechanical stress. We used the in vivo model of an aortocaval shunt (AV shunt) in adult Wistar rats to induce myocardial hypertrophy. We also used the in vitro model of cyclic stretch in rat neonatal cardiomyocytes to clarify MURC expression and the molecular regulation mechanism. The flexible membrane culture plate seeding with cardiomyocytes Cardiomyocytes seeded on a flexible membrane culture plate were stretched by vacuum pressure to 20% of maximum elongation at 60 cycles/min. AV shunt induction enhanced MURC protein expression in the left ventricular myocardium. Treatment with atorvastatin inhibited the hypertrophy induced by the AV shunt. Cyclic stretch markedly enhanced MURC protein and mRNA expression in cardiomyocytes. Addition of extracellular-signal-regulated kinase (ERK) inhibitor PD98059, ERK small interfering RNA (siRNA), angiotensin II (Ang II) antibody and atorvastatin before stretch, abolished the induction of MURC protein. An electrophoretic mobility shift assay showed that stretch enhanced the DNA binding activity of serum response factor. Stretch increased but MURC mutant plasmid, ERK siRNA, Ang II antibody and atorvastatin reversed the transcriptional activity of MURC induced by stretch. Adding Ang II to the cardiomyocytes also induced MURC protein expression. MURC siRNA and atorvastatin inhibited the hypertrophic marker and protein synthesis induced by stretch. Treatment with atorvastatin reversed MURC expression and hypertrophy under volume overload and cyclic stretch.
Identifiants
pubmed: 30511410
doi: 10.1111/jcmm.14044
pmc: PMC6349245
doi:
Substances chimiques
Anticholesteremic Agents
0
Cavin4 protein, rat
0
Muscle Proteins
0
Angiotensin II
11128-99-7
Atorvastatin
A0JWA85V8F
Extracellular Signal-Regulated MAP Kinases
EC 2.7.11.24
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1406-1414Informations de copyright
© 2018 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.
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