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Leptin protects rat cardiomyocytes from H2O2‐ and hypoxia‐induced apoptosis
Author(s) -
Shin EyunJung,
Eguchi Megumi,
Liu Yuantao,
Sweeney Gary
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1238.9
Subject(s) - leptin , medicine , apoptosis , endocrinology , hypoxia (environmental) , annexin , chemistry , mitochondrion , phosphatidylserine , cytochrome c , heart failure , reactive oxygen species , obesity , biochemistry , oxygen , membrane , phospholipid , organic chemistry
Obesity increases the risk of heart failure, yet there is also compelling evidence suggesting a protective effect of obesity on subsequent events post‐myocardial infarction. Leptin, the product of the obese ( ob ) gene, circulates at higher concentrations in obese individuals. The objective of this work was to investigate the effect of leptin on cardiomyocyte apoptosis; a well known component of cardiac remodeling that can contribute to heart failure in obesity. We used H 2 O 2 and hypoxia to mimic myocardial ischemia in vitro and first demonstrated that the decreased viability of H9c2 rat cardiomyocytes exposed to H 2 O 2 was attenuated by pretreating cells with leptin (6nM) for 1hr. Similarly, exposure to H 2 O 2 or hypoxia increased phosphatidylserine exposure as measured via annexin V binding, decreased mitochondrial membrane potential, increased cytochrome c release from mitochondria and elevated activity of caspase‐3 measured by cleavage and enzymatic assay. Importantly, all of the above were prevented when cells were pretreated with leptin for 1hr. In conclusion, we have demonstrated that leptin has anti‐apoptotic effects in rat cardiomyocytes which may be of significance in regulating the development of heart failure in obesity.