Key result
Endothelial microvesicles from adults with obesity promote a proinflammatory, proapoptotic, and NO-compromised phenotype in vitro.
Why the study?
The study was conducted to determine the effect of circulating endothelial cell-derived microvesicles isolated from adults with obesity on endothelial cell inflammation, apoptosis, and nitric oxide production in vitro.
Do circulating endothelial cell-derived microvesicles (EMVs) isolated from adults with obesity affect endothelial cell inflammation, apoptosis, and nitric oxide production in vitro?
Do circulating endothelial cell-derived microvesicles (EMVs) isolated from adults with obesity affect endothelial cell inflammation, apoptosis, and nitric oxide production in vitro?
Circulating endothelial microvesicles from adults with obesity directly promote endothelial dysfunction in vitro, suggesting a novel systemic mediator of obesity-related vascular risk.
May implicate EMVs in obesity-related vascular risk; hypothesis-generating for in vivo and clinical validation.
In the present study, we determined the effect of circulating endothelial cell-derived microvesicles (EMVs) isolated from adults with obesity on endothelial cell inflammation, apoptosis, and nitric oxide (NO) production in vitro. Circulating EMVs harvested from adults with obesity promoted a proinflammatory, proapoptotic, and NO-compromised endothelial phenotype. Elevated circulating EMVs in adults with obesity, independent of other cardiometabolic risk factors, are a potential novel systemic mediator of obesity-related endothelial dysfunction and vascular risk.
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Garcia et al. (2023) studied Obesity. Circulating endothelial cell-derived microvesicles (EMVs) was evaluated on Endothelial cell inflammation, apoptosis, and nitric oxide (NO) production in vitro. Circulating endothelial cell-derived microvesicles from adults with obesity promoted a proinflammatory, proapoptotic, and NO-compromised endothelial phenotype in vitro.
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