17beta-estradiol (E2) induced a significant increase in estrogen-responsive reporter activity and expression of specific cardiac genes in rat cardiac myocytes and fibroblasts.
Demonstrates that rat cardiac myocytes and fibroblasts contain functional estrogen receptors, providing a potential mechanism for gender-based differences in cardiovascular diseases.
Gender-based differences found in cardiovascular diseases raise the possibility that estrogen may have direct effects on cardiac tissue. Therefore we investigated whether cardiac myocytes and fibroblasts express functional estrogen receptors. Immunofluorescence demonstrated estrogen receptor protein expression in both female and male rat cardiac myocytes and fibroblasts. Nuclear translocation of the estrogen receptor protein was observed after stimulation of cardiomyocytes with 17beta-estradiol (E2). Cells transfected with an estrogen-responsive reporter plasmid showed that treatment with E2 induced a significant increase in reporter activity. Furthermore, E2 induced a significant increase in expression of the estrogen receptors alpha and beta, progesterone receptor and connexin 43 in cardiac myocytes. Cardiac myocytes and fibroblasts contain functional estrogen receptors and estrogen regulates expression of specific cardiac genes. These data suggest that gender-based differences in cardiac diseases may in part be due to direct effects of estrogen on the heart.
Grohé et al. (1997) studied Cardiovascular diseases. 17beta-estradiol (E2) was evaluated on Estrogen receptor protein expression, nuclear translocation, reporter activity, and gene expression. 17beta-estradiol (E2) induced a significant increase in estrogen-responsive reporter activity and expression of specific cardiac genes in rat cardiac myocytes and fibroblasts.