Low density lipoprotein induces upregulation of vasoconstrictive endothelin type B receptor expression

Xu, Cang‐Bao; Zheng, Jing; Zhang, Wei; Liu, Enqi; Edvinsson, Lars; Zhang, Yaping

doi:10.1016/j.vph.2013.11.004

Cited by 21 publications

(12 citation statements)

References 35 publications

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“…Acta Pharmacologica Sinica dependency on this receptor subtype in the vasoconstrictor response to this peptide [40] . However, a functional relevance of ET B receptors in vascular smooth muscle was revealed in iliac arteries from obese mice, where the ET B receptor-selective antagonist BQ-788 attenuated contractions to ET-1 in line with previous studies in hypercholesterolemic animals [41,42] . Similar to arteries of transgenic mice with endothelium-selective [32,38,43] or global overexpression of the prepro-ET-1 gene [44] , maximal contractions to ET-1 were attenuated in iliac rings from obese TET het mice.…”

Section: Wwwchinapharcom Baretella O Et Alsupporting

confidence: 87%

Endothelial overexpression of endothelin-1 modulates aortic, carotid, iliac and renal arterial responses in obese mice

Baretella

Chung

et al. 2017

Acta Pharmacol Sin

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Endothelin-1 (ET-1) is essential for mammalian development and life, but it has also been implicated in increased cardiovascular risk under pathophysiological conditions. The aim of this study was to determine the impact of endothelial overexpression of the prepro-endothelin-1 gene on endothelium-dependent and endothelium-independent responses in the conduit and renal arteries of lean and obese mice. Obesity was induced by high-fat-diet (HFD) consumption in mice with Tie-1 promoter-driven, endothelium-specific overexpression of the prepro-endothelin-1 gene (TET) and in wild-type (WT) littermates on a C57BL/6N background. Isometric tension was measured in rings (with endothelium) of the aorta (A), carotid (CA) and iliac (IA) arteries as well as the main (MRA) and segmental renal (SRA) arteries; all experiments were conducted in the absence or presence of L-NAME and/or the COX inhibitor meclofenamate. The release of prostacyclin and thromboxane A2 was measured by ELISA. In the MRA, TET per se increased contractions to endothelin-1, but the response was decreased in SRA in response to serotonin; there were also improved relaxations to acetylcholine but not insulin in the SRA in the presence of L-NAME. HFD per se augmented the contractions to endothelin-1 (MRA) and to the thromboxane prostanoid (TP) receptor agonist U46619 (CA, MRA) as well as facilitated relaxations to isoproterenol (A). The combination of HFD and TET overexpression increased the contractions of MRA and SRA to vasoconstrictors but not in the presence of meclofenamate; this combination also augmented further relaxations to isoproterenol in the A. Contractions to endothelin-1 in the IA were prevented by endothelin-A receptor antagonist BQ-123 but only attenuated in obese mice by BQ-788. The COX-1 inhibitor FR122047 abolished the contractions of CA to acetylcholine. The release of prostacyclin during the latter condition was augmented in samples from obese TET mice and abolished by FR122047. These findings suggest that endothelial TET overexpression in lean animals has minimal effects on vascular responsiveness. However, if comorbid with obesity, endothelin-1-modulated, prostanoid-mediated renal arterial dysfunction becomes apparent.

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Section: Wwwchinapharcom Baretella O Et Alsupporting

confidence: 87%

Endothelial overexpression of endothelin-1 modulates aortic, carotid, iliac and renal arterial responses in obese mice

Baretella

Chung

et al. 2017

Acta Pharmacol Sin

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“…The arteries (without endothelium) were cut into 1 mm long cylindrical segments and mounted to a myograph system (620 M, Danish Myo Technology A/S, Aarhus, Denmark) for recording the receptor-mediated vasoconstriction. The concentration-response curves (CRCs) were performed by cumulative administration of selective ET B agonist sarafotoxin 6c (S6c, Sigma-Aldrich, Saint Louis, MO, USA), followed by nonselective ETR agonist ET-1 (Calbiochem, La Jolla, CA, USA), as previously described [6, 11]. Briefly, after S6c CRCs were obtained, the arterial rings were coincubated with S6c (10 −7.5 M) for 30 min.…”

Section: Methodsmentioning

confidence: 99%

“…Elongation factor-1 (EF-1, Eef1a1, GenBank accession no. NM_175838) mRNA was used as reference (internal control) [5, 11]. The primers were forward 5′-GCAAGCCCATGTGTGTTGAA-3′ and reverse 5′-TGATGACACCCACAGCAACTG-3′.…”

Section: Methodsmentioning

confidence: 99%

Enhanced Endothelin A and B Receptor Expression and Receptor-Mediated Vasoconstriction in Rat Mesenteric arteries after Lipopolysaccharide Challenge

Zhang

Huang

et al. 2019

Mediators of Inflammation

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During organ culture of intact vessels, endothelin receptors (ETRs) were upregulated in vascular smooth muscle cells (VSMCs) by various stimuli, but whether inflammation alters ETR expression in vivo remains unclear. We aimed to explore the effects of lipopolysaccharide (LPS) challenge on ETR expression in the VSMC in vivo. Male Sprague-Dawley rats received a single intraperitoneal injection of LPS (5 mg/kg body weight) or normal saline (NS) for 6 hrs. The function and expression of ETR type A (ETA) and type B (ETB) were evaluated in the mesenteric arteries without endothelium, by using myograph system, real-time quantitative PCR, Western blot, and immunohistochemical staining, respectively. Serum tumor necrosis factor-α (TNF-α) level was assessed by using enzyme-linked immunosorbent assay. The results showed that, compared to control (NS) group, LPS treatment potently enhanced the vasoconstriction mediated by ETA or ETB in rat mesenteric artery, with elevated maximum effects. ETA and ETB expressions in the VSMC were increased at both mRNA and protein levels after LPS treatment, paralleled with activation of the NF-κB pathway and augmented serum TNF-α level. Conclusively, in the rat model of immediate systemic inflammation induced by LPS, ETA and ETB expressions were increased in the mesenteric arterial VSMC, paralleled with enhanced receptor-mediated vasoconstriction and activation of the NF-κB pathway. Our data has for the first time demonstrated the upregulation of ETRs in VSMCs by LPS-induced immediate inflammation in vivo.

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“…TNF, interleukins 1, 6 and 8 and GCM-CSF) and enhances neutrophil adhesion to the arterial endothelium [7]. These studies implicate that these effects promote vascular inflammation and atherosclerosis, ET-1 being a key mediator in this context [2,10,33,34]. This assumption is underscored by experimental data from Ihling et al [35], which indicated that ET-1 levels are already significantly raised in fatty streaks, the very early stage of the atherosclerotic plaque.…”

Section: Discussionmentioning

confidence: 95%

Plasma endothelin-1 and cardiovascular risk among young and healthy adults

et al. 2015

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Low density lipoprotein induces upregulation of vasoconstrictive endothelin type B receptor expression

Cited by 21 publications

References 35 publications

Endothelial overexpression of endothelin-1 modulates aortic, carotid, iliac and renal arterial responses in obese mice

Endothelial overexpression of endothelin-1 modulates aortic, carotid, iliac and renal arterial responses in obese mice

Enhanced Endothelin A and B Receptor Expression and Receptor-Mediated Vasoconstriction in Rat Mesenteric arteries after Lipopolysaccharide Challenge

Plasma endothelin-1 and cardiovascular risk among young and healthy adults

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