ArticleMicrocirculation (New York, N.Y. : 1994)2012
CYP2C29 produces superoxide in response to shear stress.
Article in Microcirculation (New York, N.Y. : 1994), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Endothelial deletion of the cytochrome P450 reductase leads to cardiac remodelling.Frontiers in physiology · 2022Article
- EETs Elicit Direct Increases in Pulmonary Arterial Pressure in Mice.American journal of hypertension · 2016Article
- Sexually dimorphic phenotype of arteriolar responsiveness to shear stress in soluble epoxide hydrolase-knockout mice.American journal of physiology. Heart and circulatory physiology · 2015Article
- Soluble epoxide hydrolase-dependent regulation of myogenic response and blood pressure.American journal of physiology. Heart and circulatory physiology · 2014Article
- Reciprocal actions of constrictor prostanoids and superoxide in chronic hypoxia-induced pulmonary hypertension: roles of EETs.Pulmonary circulationArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
objectiveActivation of CYP2C29 releases superoxide during shear stress-induced dilation (SSID).
methodsMesenteric arteries isolated from female eNOS-KO and WT mice were cannulated and pressurized. Vasodilation and superoxide production in response to shear stress were assessed.
resultsShear stress-induced dilation was significantly attenuated in vessels of eNOS-KO compared with WT mice, which was normalized by tempol and PEG-Catalase, in a PPOH (inhibitor of CYP2C29)-sensitive manner, but remained unaffected by VAS2870 and allopurinol, inhibitors of NADPH oxidase and xanthine oxidase, respectively. NaNO(2)-induced dilation was comparable in both strains of mice. Confocal microscopy shows that SS-stimulated superoxide was increased particularly in the endothelium of eNOS-KO mice. HPLC analysis of 2-EOH indicated an increase in SS-stimulated superoxide in vessels of eNOS-KO mice, a response that was sensitive to PPOH. Inhibition of soluble epoxide hydrolase significantly enhanced SSID without affecting SS-stimulated superoxide production. CYP2C29 and catalase were upregulated, and exogenous H(2)O(2) caused vasoconstriction in vessels of eNOS-KO mice.
conclusionsCYP2C29 synthesizes EETs to mediate SSID, and simultaneously releases superoxide and sequential H(2)O(2), which in turn impair SSID.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.