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- W815513883 abstract "Obesity is associated with recruitment of macrophages to the microvascular adventitia. The current objective was to define how macrophage-derived signals contribute to microvascular dysfunction. Based on recent findings that impaired H2S signaling is associated with cardiovascular pathologies, it was hypothesized that in the diet-induced mouse model of obesity microvascular H2S is depleted by a mechanism that involves interactions with perivascular macrophages. Mesenteric arterioles were isolated from 30 week-old lean and obese mice and mounted for pressure myography. Vessels were loaded with the H2S indicator SF7-AM and imaged using confocal microscopy. Obesity was associated with lower H2S levels in both the smooth muscle and endothelial layers. Generation of H2S is dependent on the substrate L-cysteine and the enzyme cystathionine gamma-lyase (CSE). Expression of CSE was not changed by obesity; however, L-cysteine was less effective in evoking H2S production in these vessels, and was correlated with reduced relaxation when pre-contracted with phenylephrine. Co-culturing arterioles from lean mice overnight with peritoneal macrophages from obese mice resulted in vessel H2S depletion. In contrast, co-culture of vessels from either lean or obese mice with macrophages from lean controls had no effects on vessel H2S. Taken together, these data support a model in which H2S biosynthesis is compromised in the obese microvasculature by a mechanism dependent on crosstalk with perivascular macrophages. Supported by the American Heart Association and a Chicago Medical School/Advocate Lutheran General Hospital Pilot Grant." @default.
- W815513883 created "2016-06-24" @default.
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- W815513883 date "2015-04-01" @default.
- W815513883 modified "2023-10-16" @default.
- W815513883 title "Macrophages Cause Reduced Biosynthesis of Hydrogen Sulfide in the Obese Microvasculature" @default.
- W815513883 doi "https://doi.org/10.1096/fasebj.29.1_supplement.636.2" @default.
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