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- W3170093318 abstract "A critical amount of reactive oxygen species (ROS) contributes to coronary blood flow (CBF) regulation; however, oxidative stress impairs CBF regulation. We have previously demonstrated TRPV1-dependent coupling of CBF to metabolism is disrupted in diabetic cardiomyopathy (DCM). Accordingly, we hypothesized that basal levels of H2O2 stimulate TRPV1 whereas enhanced oxidative stress desensitizes TRPV1 via an H2O2 dependent post translational modification involving the lipid peroxidation product 4-Hydroxynonenal (4-HNE). Using contrast echocardiography, H2O2 dose-dependently increased CBF in control and TRPV1−/− mice, yet was greater in controls compared to TRPV1−/−. Similarly, H2O2 potentiated capsaicin-mediated CBF increases in controls. H2O2 caused robust dilation in control coronary microvessels (blunted in the presence of the TRPV1 inhibitor SB366791 and in TRPV1−/− vessels), suggesting H2O2 induced vasodilation occurs in part via TRPV1. H2O2 induced Ca2+ influx was TRPV1 dependent in HEK and TRPV1−/− endothelial cells (ECs) transfected with TRPV1 and further verified using Ca2+ imaging and electrophysiology. Lastly, ECs incubated with H2O2 (1hr) and 4- HNE (1hr) demonstrated increased 4-HNE levels and 4-HNE modified TRPV1 via western/co-immunoprecipitation. These data suggest low levels of H2O2 can potentiate TRPV1 however, increased ROS concentrations as seen in DCM can lead to enhanced 4-HNE levels which modulate TRPV1 and disrupt its signaling, resulting in tissue perfusion impairments." @default.
- W3170093318 created "2021-06-22" @default.
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- W3170093318 date "2013-04-01" @default.
- W3170093318 modified "2023-09-27" @default.
- W3170093318 title "ROS‐induced membrane lipid peroxidation impairs TRPV1 channels in the vasculature" @default.
- W3170093318 doi "https://doi.org/10.1096/fasebj.27.1_supplement.913.48" @default.
- W3170093318 hasPublicationYear "2013" @default.
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