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1Cardiology Research, Veterans Affairs Medical Center and Baylor College of Medicine, Houston 77030; 2Michael E. DeBakey Institute for Comparative Cardiovascular Science and 3Department of Veterinary Physiology and Pharmacology, Texas A&M University, College Station, Texas 77843; 4Department of Physiology and Cardiovascular Research Institute, Maastricht University, 6200 MD Maastricht, the Netherlands; and 5Department of Anesthesiology and Intensive Care Medicine, University of Bonn, Bonn, D-53012 Germany
Submitted 25 November 2002 ; accepted in final form 17 April 2003
The heat shock proteins (HSPs) are an important family of endogenous,
protective proteins that are found in all tissues. In the heart, HSP72, the
inducible form of HSP70, has been the most intensely studied. It is well
established that HSP72 is induced with ischemia and is cardioprotective.
Overexpression of other HSPs also is protective against cardiac injury.
Recently, we observed that 17
-estradiol increases levels of HSPs in male
rat cardiac myocytes. We hypothesized that there were gender differences in
HSP72 expression in the heart secondary to estrogen. To test this hypothesis,
we examined cardiac levels of HSP72 by ELISA in male and female Sprague-Dawley
rats. In addition, three other HSPs were assessed by Western blot (HSP27,
HSP60, and HSP90). To determine whether estrogen status affected HSP72
expression in other muscles or tissues, two other muscle tissues, slow twitch
muscle (soleus muscle) and fast twitch muscle (gastrocnemius muscle), were
studied as well as two other organs, the kidney and liver. Because HSP72 is
cardioprotective, and females are known to have less cardiovascular disease
premenopause, the effects of ovariectomy were examined. We report that female
Sprague-Dawley rat hearts have twice as much HSP72 as male hearts. Ovariectomy
reduced the level of HSP72 in female hearts, and this could be prevented by
estrogen replacement therapy. These data show that the expression of cardiac
HSP72 is greater in female rats than in male rats, due to upregulation by
estrogen.
hormones; cardiovascular diseases; ischemia
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