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Anoxia/reoxygenation‐induced cardiac myocyte apoptosis: role of HMGB1
Author(s) -
Yang Min,
Wu Jun,
Martin Claudio,
Rui Tao
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.730.30
Subject(s) - myocyte , apoptosis , cardiac myocyte , hmgb1 , programmed cell death , microbiology and biotechnology , biology , medicine , biochemistry , receptor
It has been proposed that ischemia/reperfusion (I/R)‐induced myocardial dysfunction is due to myocytes apoptosis. However, the mechanism(s) involved in myocyte apoptosis after I/R is not completely clear, but appears to involve cytokines. High mobility group box 1 (HMGB1) is a nuclear non‐histone DNA binding protein that has been implicated in cell apoptosis. The aim of the present study was to assess the role of HMGB1 in myocyte apoptosis‐induced by anoxia/reoxygenation (A/R, in vitro counter part of I/R). Cultured murine cardiac myocytes were challenged with a 30 min of anoxia followed by 48 hrs of reoxygenation. The A/R challenge increased myocyte apoptosis (Caspase 3 activity and Cell Death ELISA). Concomitantly, there was an increase in HMGB1 expression in cardiac myocytes. Further, the A/R‐induced increase in myocyte apoptosis was prevented when the myocytes were pretreated with a HMGB1 inhibitor (glycyrrhizic acid). Finally, exposure of the cardiac myocytes to medium containing HMGB1 (1 μg/ml) for 24 hrs resulted in myocyte apoptosis. Taken together, our findings indicate that HMGB1 production by cardiac myocytes plays an important role in A/R‐induced myocyte apoptosis. (CIHR MOP 81303).