Key result
Treatment of cultured human aortic endothelial cells with 17 beta-estradiol enhanced calcium-dependent NO production and increased NO synthase protein levels, whereas testosterone had no effect.
Why the study?
Does 17 beta-estradiol increase NO production and NO synthase protein levels in cultured human aortic endothelial cells?
Does 17 beta-estradiol increase NO production and NO synthase protein levels in cultured human aortic endothelial cells?
17 beta-estradiol up-regulates endothelial nitric oxide synthase and enhances NO production in human aortic endothelial cells, providing a potential mechanism for estrogen's cardiovascular effects.
Suggests estrogen's vascular mechanism in vitro; hypothesis-generating for clinical translation pending human studies.
We have examined the effects of sex hormones on calcium-dependent NO production and protein levels of NO synthase in cultured human aortic endothelial cells, which were treated with various doses of 17 beta-estradiol and testosterone for 8-48 h. Treatment with 17 beta-estradiol enhanced calcium-dependent NO production, but testosterone had exerted no effect. Western blot using monoclonal anti-human endothelial NO synthase antibody clarified that increased NO production by 17 beta-estradiol treatment was accompanied by increased NO synthase protein. Our results provide evidence that human endothelial NO synthase can be regulated by estrogens.
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Hishikawa et al. (1995) studied Cultured human aortic endothelial cells. 17 beta-estradiol vs. testosterone was evaluated on calcium-dependent NO production and protein levels of NO synthase. Treatment of cultured human aortic endothelial cells with 17 beta-estradiol enhanced calcium-dependent NO production and increased NO synthase protein levels, whereas testosterone had no effect.
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