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- W1569436995 abstract "Microvessels are dynamic complexes of vascular structures, formed elements of blood carried by plasma, parenchymal cells, and the interstitial matrix through which they course. Only recently how these elements interrelate to maintain homeostasis differently, often subtly, in females (F) and males (M) is being studied and the implications recognized. We tested the hypothesis that the phenotype of the endothelial cells (EC) lining the vasculature, known to differ by organ and vessel type, would not differ with sex. EC isolated from the aorta and microvasculature of skeletal muscle (SKM) and mesentery (MES) of F and M adult rats were studied with respect to morphology, growth, metabolism and mechanics. We rejected our hypothesis as profound sex-differences existed for each EC source. For example, F aortic EC were smaller (13 vs 16 μm) and their numbers in culture were greater than M; in SKM and MES F>M (16 vs 15 and 18 vs 15 μm, respectively). Sex and tissue differences were noted for VE Cadherin, eNOS, Insulin receptor β, androgen receptor, and estrogen receptor α and β expression. With respect to fiber orientation and frequency as assessed by atomic force microscopy, overall actin fiber orientation converged in one direction more uniformly in F than M and differed by tissue source. While aortic EC lactate production was sex-independent, F<M for microvessel EC. Understanding sexual dimorphism in EC will assist in delineating the sources of sex-differences that influence both the incidence and severity of disease Grant Funding Source: Supported by NIH DK 095501 and MU Div of Pulm & Critical Care Medicine" @default.
- W1569436995 created "2016-06-24" @default.
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- W1569436995 date "2014-04-01" @default.
- W1569436995 modified "2023-10-16" @default.
- W1569436995 title "Influence of sexual dimorphism on endothelial morphology, metabolism and mechanics (680.18)" @default.
- W1569436995 doi "https://doi.org/10.1096/fasebj.28.1_supplement.680.18" @default.
- W1569436995 hasPublicationYear "2014" @default.
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