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Gender modulation of cardiac gene expression in rats with chronic volume overload
Author(s) -
Walton Karen L.,
McLarty Jennifer L.,
Bennett Shante',
Melendez Giselle C.,
SaboAttwood Tara,
Brower Gregory L.
Publication year - 2009
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.23.1_supplement.362.6
Subject(s) - endocrinology , medicine , volume overload , gene expression , ventricular remodeling , heart failure , inflammation , biology , gene , biochemistry
We have previously described gender differences in cardiac remodeling secondary to chronic volume overload in rats. However, the mechanisms underlying ovarian hormone mediated cardioprotection have not yet been elucidated. Accordingly, this study sought to identify altered cardiac gene expression contributing to the protection from adverse cardiac remodeling seen in female rats. To that end, left ventricular (LV) gene expression in male and intact and ovariectomized adult female rats (N=3 per group) with an aortocaval fistula was compared to sham‐operated controls. At three days post‐surgery, the hearts were excised, separated and the LV prepared for RNA isolation. An Applied Biosystems Low Density Inflammation Array allowed us to simultaneously examine 96 genes of interest. There were significant gender differences observed in the expression of genes kallikrein‐15, cyclooxgenase‐1 and ‐2, thromboxane synthases and nerve growth factor which were subsequently confirmed by RT‐PCR. Cytokine gene expression, including the TNF‐alpha superfamily, IL‐6 and stem cell factor were also similarly affected. Thus, ovarian hormone regulation of prostaglandin, cytokine and serine protease inflammatory gene expression in the heart are implicated in the attenuation of pathogenic remodeling induced by a chronic volume overload. Funding Sources: NIH grants RO1‐HL‐62228 and RO1‐HL‐073990