NDLI: Glucosamine Protects Neonatal Cardiomyocytes from Ischemia-Reperfusion Injury via increased protein O-GlcNAc and increased mitochondrial Bcl-2

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Glucosamine Protects Neonatal Cardiomyocytes from Ischemia-Reperfusion Injury via increased protein O-GlcNAc and increased mitochondrial Bcl-2

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Champattanachai, Voraratt Marchase, Richard B. Chatham, John C.
Description	Country affiliation: United States Author Affiliation: Champattanachai V ( Department of Cell Biology, University of Alabama at Birmingham, Birmingham, AL 35294-0005, USA.)
Abstract	We have previously reported that glucosamine protected neonatal rat ventricular myocytes against ischemia-reperfusion (I/R) injury, and this was associated with an increase in protein O-linked-N-acetylglucosamine (O-GlcNAc) levels. However, the protective effect of glucosamine could be mediated via pathways other that O-GlcNAc formation; thus the initial goal of the present study was to determine whether increasing O-GlcNAc transferase (OGT) expression, which catalyzes the formation of O-GlcNAc, had a protective effect similar to that of glucosamine. To better understand the potential mechanism underlying O-GlcNAc-mediated cytoprotection, we examined whether increased O-GlcNAc levels altered the expression and translocation of members of the Bcl-2 protein family. Both glucosamine (5 mM) and OGT overexpression increased basal and I/R-induced O-GlcNAc levels, significantly decreased cellular injury, and attenuated loss of cytochrome c. Both interventions also attenuated the loss of mitochondrial membrane potential induced by H2O2 and were also associated with an increase in mitochondrial Bcl-2 levels but had no effect on Bad or Bax levels. Compared with glucosamine and OGT overexpression, NButGT (100 microM), an inhibitor of O-GlcNAcase, was less protective against I/R and H2O2 and did not affect Bcl-2 expression, despite a 5- to 10-fold greater increase in overall O-GlcNAc levels. Decreased OGT expression resulted in lower basal O-GlcNAc levels, prevented the I/R-induced increase in O-GlcNAc and mitochondrial Bcl-2, and increased cellular injury. These results demonstrate that the protective effects of glucosamine are mediated via increased formation of O-GlcNAc and suggest that this is due, in part, to enhanced mitochondrial Bcl-2 translocation.
File Format	HTM / HTML
ISSN	03636143
e-ISSN	15221563
DOI	10.1152/ajpcell.00456.2007
Journal	American Journal of Physiology - Cell Physiology
Issue Number	6
Volume Number	294
Language	English
Publisher	American Physiological Society
Publisher Date	2008-06-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Cell Biology Acetylglucosamine Metabolism Glucosamine Mitochondria, Heart Myocardial Reperfusion Injury Prevention & Control Myocytes, Cardiac Protein Processing, Post-translational Proto-oncogene Proteins C-bcl-2 Animals Animals, Newborn Cell Survival Cells, Cultured Cytochromes c Cytoprotection Enzyme Inhibitors Pharmacology Glycosylation Hydrogen Peroxide Membrane Potential, Mitochondrial Drug Effects Enzymology Pathology N-acetylglucosaminyltransferases Genetics Protein Transport Rna Interference Rats, Sprague-dawley Transfection Up-regulation Beta-n-acetylhexosaminidases Antagonists & Inhibitors Research Support, N.i.h., Extramural
Content Type	Text
Resource Type	Article
Subject	Cell Biology Physiology

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