References of "Karas, R. H"
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See detailEffects of estrogen on skeletal myoblast growth.
Kahlert, S.; Grohe, C.; Karas, R. H. et al

in Biochemical and biophysical research communications (1997), 232(2), 373-8

To determine the role of estrogen in skeletal muscle growth, we investigated estrogen receptor-mediated effects on proliferation in skeletal myoblasts. In L6, C2C12 and Sol8 myoblasts estrogen receptor ... [more ▼]

To determine the role of estrogen in skeletal muscle growth, we investigated estrogen receptor-mediated effects on proliferation in skeletal myoblasts. In L6, C2C12 and Sol8 myoblasts estrogen receptor was demonstrated by immunoblotting, immunofluorescence microscopy and transfection studies. Estrone induced a significant increase in myoblast growth whereas 17 beta-estradiol had no effect. Furthermore in L6-cells estrone (c-fos: 3.9-fold, egr-1: 4.6-fold) induced immediate-early gene induction significantly stronger than 17 beta-estradiol (c-fos: 1.7-fold, egr-1: 2.3-fold; p < 0.05). Skeletal myoblasts express functional estrogen receptors. Estrogens differ in the activation of skeletal myoblast growth and immediate-early gene induction. [less ▲]

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See detailCardiac myocytes and fibroblasts contain functional estrogen receptors.
Grohe, C.; Kahlert, S.; Lobbert, K. et al

in FEBS letters (1997), 416(1), 107-12

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 ... [more ▼]

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. [less ▲]

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