Role of adiponectin receptors in endothelin-induced cellular hypertrophy in cultured cardiomyocytes and their expression in infarcted heart
Abstract
Adiponectin, an adipocyte-derived protein, has cardioprotective actions. We elucidated the role of the adiponectin receptors AdipoR1 and AdipoR2 in the effects of adiponectin on endothelin-1 (ET-1)-induced hypertrophy in cultured cardiomyocytes, and we examined the expression of adiponectin receptors in normal and infarcted mouse hearts. Recombinant full-length adiponectin suppressed the ET-1-induced increase in cell surface area and [3 H]leucine incorporation into cultured cardiomyocytes compared with cells treated with ET-1 alone. Transfection of small interfering RNA (siRNA) specific for AdipoR1 or AdipoR2 reversed the suppressive effects of adiponectin on ET-1-induced cellular hypertrophy in cultured cardiomyocytes. Adiponectin induced phosphorylation of AMP-activated protein kinase (AMPK) and inhibited ET-1-induced ERK1/2 phosphorylation, which were also reversible by transfection of siRNA for AdipoR1 or AdipoR2 in cultured cardiomyocytes. Transfection of siRNA for α 2-catalytic subunits of AMPK reduced the inhibitory effects of adiponectin on ET-1-induced cellular hypertrophy and ERK1/2 phosphorylation. Effects of globular adiponectin were similar to those of full-length adiponectin, and siRNA for AdipoR1 reversed the actions of globular adiponectin. Compared with normal left ventricle, expression levels of AdipoR1 mRNA and protein were decreased in the remote, as well as the infarcted, area after myocardial infarction in mouse hearts. In conclusion, AdipoR1 and AdipoR2 mediate the suppressive effects of full-length and globular adiponectin on ET-1-induced hypertrophy in cultured cardiomyocytes, and AMPK is involved in signal transduction through these receptors. AdipoR1 and AdipoR2 might play a role in the pathogenesis of ET-1-related cardiomyocyte hypertrophy after myocardial infarction.
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Both full-length and globular adiponectin attenuated endothelin (ET)-1-induced hypertrophy in cultured cardiomyocytes, suggesting a potential role in the pathogenesis of ET-1-related cardiomyocyte hypertrophy after MI.
“Thus, whereas adiponectin may mediate a direct in vitro hypertrophic effect on primary cardiomyocytes (320), another study showed that both full-length and globular adiponectin attenuated endothelin (ET)-1-induced hypertrophy in cultured cardiomyocytes, suggesting a potential role in the pathogenesis of ET-1-related cardiomyocyte hypertrophy after MI (108).”
From Cardiac remodeling in obesity (2008) · cites this paper as [108]
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- Authors
- Fujioka, D., Kawabata, K.-I., Saito, Y., Kobayashi, T., Nakamura, T., Kodama, Y., Takano, H., Obata, J.-E., Kitta, Y., Umetani, K., & Kugiyama, K.
- Affiliations
- University of Yamanashi (JP)
- ORCID
- Venue
- American Journal of Physiology-Heart and Circulatory Physiology
- Publisher
- American Physiological Society
- Published
- 2006-06
- Volume
- 290
- Issue
- 6
- Pages
- H2409-H2416
- ISSN
- 0363-6135 (ISSN-L)
- 1522-1539
- OpenAlex
- W2104692150
- Cited by
- 115
- References
- 23
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 1 · 2023: 3 · 2022: 2 · 2021: 4 · 2020: 2 · 2019: 3 · 2018: 4 · 2017: 3 · 2016: 5 · 2015: 4 · 2014: 8 · 2013: 6 · 2012: 9
- FWCI
- 7.81
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Keywords
- adiponectin, adiponectin receptors, AdipoR1, AdipoR2, endothelin-1, cardiomyocyte hypertrophy, myocardial infarction, AMPK, ERK1/2 phosphorylation, globular adiponectin, cardioprotection
- MeSH terms
- Angiotensin II, Animals, Cells, Cultured, Cardiomegaly, Image Processing, Computer-Assisted, Immunohistochemistry, Myocardial Infarction, Norepinephrine, Receptors, Cell Surface, RNA, Messenger, Transfection, Tumor Necrosis Factor-alpha, Endothelins, Rats, Sprague-Dawley, Neurotransmitter Agents, Endothelin-1, Myocytes, Cardiac, RNA, Small Interfering, Rats, Adiponectin, Receptors, Adiponectin
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