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Kwon, H. Moo
Inflammation and Kidney Disorder Lab
Research Interests
  • TonEBP, Obesity, Cancer, Chronic inflammatory diseases, Brain disorder, Kidney disorders, Genomic instability

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Reactive oxygen species inhibit hyposmotic stress-dependent volume regulation in cultured rat cardiomyocytes

Cited 13 times inthomson ciCited 10 times inthomson ci
Title
Reactive oxygen species inhibit hyposmotic stress-dependent volume regulation in cultured rat cardiomyocytes
Author
Diaz-Elizondo, JessicaChiong, MarioRojas-Rivera, DiegoOlea-Azar, ClaudioKwon, H. MooLavandero, Sergio
Keywords
hyposmotic stress; reactive oxygen species; volume regulation; cardiomyocytes; heart
Issue Date
200612
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Citation
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.350, no.4, pp.1076 - 1081
Abstract
Cells have developed compensatory mechanisms to restore cell volume, and the ability to resist osmotic swelling or shrinkage parallels their resistance to necrosis or apoptosis. There are several mechanisms by which cells adapt to hyposmotic stress including that of regulatory volume decrease. In ischemia and reperfusion, cardiomyocytes are exposed to hyposmotic stress, but little is known as to how their volume is controlled. Exposure of cultured neonatal rat cardiomyocytes to hyposmotic media induced a rapid swelling without any compensatory regulatory volume decrease. The hyposmotic stress increased the production of reactive oxygen species, mainly through NADPH oxidase. Adenoviral overexpression of catalase inhibited the hyposmosis-dependent OH production, induced the regulatory volume decrease mechanism, and prevented cell death. These results suggest that hyposmotic stress of cardiomyocytes stimulates production of reactive oxygen species which are closely linked to volume regulation and cell death.
URI
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DOI
http://dx.doi.org/10.1016/j.bbrc.2006.10.004
ISSN
0006-291X
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