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Cardiology Research, Veterans Affairs Medical Center and Baylor College of Medicine, Houston, Texas 77030
Heat-shock proteins (HSPs) are an important family of
endogenous protective proteins, which increase in response to
myocardial ischemia and other stresses. Overexpression of HSP72
is cardioprotective. We were interested in the regulation of heat-shock
factor (HSF), the transcription factor for HSP genes. Previously we
have observed that the inflammatory cytokine tumor necrosis factor-
increases HSP72 levels and postulated that dexamethasone might effect
the heat shock response. In the adult rat cardiac myocyte we found that
treatment with either low (10 µM)- or high (100 µM)-dose dexamethasone activated HSF by 2-6 h as determined by gel shift assay without evidence of cytotoxicity. Although HSF activation is a
key step in expression of HSP72, this may not result in an increase in
HSP72. We found that 10 µM dexamethasone increased HSP72 38%, and
100 µM dexamethasone increased HSP72 62% (P < 0.05). HSP27
and HSP60 were unchanged. The selective increase in HSP72 was
associated with protection of the cardiac myocytes from hypoxia and
reoxygenation. We conclude that dexamethasone is a novel inducer of the
heat shock response.
glucocorticoids; heat-shock factor; ischemia
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