Aryl hydrocarbon receptor (AhR) activation contributes to high-fat diet-induced vascular dysfunction.

التفاصيل البيبلوغرافية
العنوان:	Aryl hydrocarbon receptor (AhR) activation contributes to high-fat diet-induced vascular dysfunction.
المؤلفون:	da Silva JF; Department of Pharmacology, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto, Brazil., Bolsoni JA; Department of Pharmacology, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto, Brazil., da Costa RM; Department of Pharmacology, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto, Brazil.; Academic Unit on Health Sciences, Jataí Federal University, Jataí, Brazil., Alves JV; Department of Pharmacology, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto, Brazil., Bressan AFM; Department of Pharmacology, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto, Brazil., Silva LEV; Department of Physiology, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto, Brazil., Costa TJ; Department of Pharmacology, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto, Brazil., Oliveira AER; Department of Pharmacology, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto, Brazil.; Department of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of São Paulo, São Paulo, Brazil., Manzato CP; Department of Pharmacology, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto, Brazil., Aguiar CA; Department of Physiology, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto, Brazil., Fazan R Jr; Department of Physiology, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto, Brazil., Cunha FQ; Department of Pharmacology, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto, Brazil., Nakaya HI; Department of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of São Paulo, São Paulo, Brazil.; Israelita Albert Einstein Hospital, São Paulo, Brazil., Carneiro FS; Department of Pharmacology, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto, Brazil., Tostes RC; Department of Pharmacology, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto, Brazil.
المصدر:	British journal of pharmacology [Br J Pharmacol] 2022 Jun; Vol. 179 (12), pp. 2938-2952. Date of Electronic Publication: 2022 Feb 17.
نوع المنشور:	Journal Article; Research Support, Non-U.S. Gov't
اللغة:	English
بيانات الدورية:	Publisher: Wiley Country of Publication: England NLM ID: 7502536 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1476-5381 (Electronic) Linking ISSN: 00071188 NLM ISO Abbreviation: Br J Pharmacol Subsets: MEDLINE
أسماء مطبوعة:	Publication: London : Wiley Original Publication: London, Macmillian Journals Ltd.
مواضيع طبية MeSH:	Diet, High-Fat/adverse effects , Receptors, Aryl Hydrocarbon/genetics , Receptors, Aryl Hydrocarbon*/metabolism, Animals ; Endothelial Cells/metabolism ; Endothelium, Vascular ; Male ; Mice ; Mice, Inbred C57BL ; Obesity/metabolism ; Vasodilation/physiology
مستخلص:	Background and Purpose: Metabolic and vascular dysfunction are common features of obesity. Aryl hydrocarbon receptor (AhR) regulates lipid metabolism and vascular homeostasis, but whether vascular AhR are activated in obesity or have a protective and/or harmful effects on vascular function in obesity are unknown. Our study addresses whether AhR activation contributes to obesity-associated vascular dysfunction and the mechanisms involved in these AhR effects. Experimental Approach: Male AhR KO (Ahr ^-/- ) and WT mice were fed either control or a HF (high-fat) diet for 10 weeks. Metabolic and inflammatory parameters were measured in serum and adipose tissue. Vascular reactivity (isometric force) was evaluated using a myography. Endothelial NOS (eNOS) and AhR protein expression was determined by western blot, Cyp1A1 and Nos3 gene expression by RT-PCR and.NO production was quantified by DAF fluorescence. Key Results: HF diet increased total serum HDL and LDL, as well as vascular AhR protein expression and proinflammatory cytokines in the adipose tissue. HF diet decreased endothelium-dependent vasodilation. AhR deletion protected mice from HF diet-induced dyslipidaemia, weight gain and inflammatory processes. HF diet-induced endothelial dysfunction was attenuated in Ahr ^-/- mice. Vessels from Ahr ^-/- mice exhibited a greater NO reserve. In cultured endothelial cells, lysophosphatidylcholine (LPC) a major component of LDL and oxidized LDL [oxLDL]) reduced Nos3 gene expression and NO production. Antagonism of the AhR inhibited LPC effects on endothelial cells and induced decreased endothelium-dependent vasodilation. Conclusion and Implications: AhR deletion attenuates HF diet-induced dyslipidaemia and vascular dysfunction by improving eNOS/NO signalling. Targeting AhRs may prevent obesity-associated vascular dysfunction. (© 2022 The British Pharmacological Society.)
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فهرسة مساهمة:	Keywords: AhR; Aryl hydrocarbon receptors; cardiovascular diseasedyslipidaemiaendotheliumNOobesity
المشرفين على المادة:	0 (Receptors, Aryl Hydrocarbon)
تواريخ الأحداث:	Date Created: 20220103 Date Completed: 20220517 Latest Revision: 20220531
رمز التحديث:	20221213
DOI:	10.1111/bph.15789
PMID:	34978070
قاعدة البيانات:	MEDLINE

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تدمد:	1476-5381
DOI:	10.1111/bph.15789