Gender medicine: human male and female endothelial cells are different
All the common cardiovascular risk factors (smoking, hypercholesterolemia, hypertension, obesity, diabetes) trigger an impairment in endothelial function with a decrease in nitric oxide (NO) formation due to a reduced endothelial Nitric Oxide Synthase (eNOS) activity. NO plays important roles in the control of several endothelial functions such as vessel dilation, leukocyte adhesion, platelet aggregation, and angiogenesis. By independently studying human male and female endothelial cells, this study demonstrates that female endothelial cells express higher eNOS levels that are associated to a higher NO production. The female capability to generate more NO than the male counterpart may be implicated in the protection against cardiovascular diseases characterizing the young female population.
Interestingly, the increased female eNOS expression is already present at birth, thus suggesting an inborn genetic/epigenetic regulation of this feature, and supporting the hypothesis that endothelial cells have a sex.
Biological sex is still under investigated in preclinical and in vitro experiments, even when sex-dependent pathologies are studied. Our results, providing new insights in sex-specific properties of endothelial cells, may implement sex-related differences into health care strategies. A better understanding of endothelial cell dimorphisms and of their mechanisms may further suggest new targets for the design of more precise preventive and therapeutic strategies for diseases associated to an impaired endothelial function.
Sex-specific eNOS activity and function in human endothelial cells.
Sci Rep. 2017 Aug 29;7(1):9612. doi: 10.1038/s41598-017-10139-x.