Apolipoprotein B of low-density lipoprotein impairs nitric oxide-mediated endothelium-dependent relaxation in rat mesenteric arteries

Zhang, Yaping; Zhang, Wei; Edvinsson, Lars; Xu, Cang‐Bao

doi:10.1016/j.ejphar.2014.01.008

Cited by 13 publications

(7 citation statements)

References 36 publications

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“…Previous studies point for a close association between a decreased endothelium-dependent relaxation and an elevated content of oxidized LDL [4,46–48]. We demonstrate here that LPI and LPC strongly suppress the hyperpolarization of cultured EC stimulated with histamine.…”

Section: Discussionsupporting

confidence: 79%

GPR55 agonist lysophosphatidylinositol and lysophosphatidylcholine inhibit endothelial cell hyperpolarization via GPR-independent suppression of Na+-Ca2+ exchanger and endoplasmic reticulum Ca2+ refilling

Bondarenko

Montecucco

Panasiuk

et al. 2017

Vascular Pharmacology

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Lysophosphatidylinositol (LPI) and lysophosphatidylcholine (LPC) are lipid signaling molecules that induce endothelium-dependent vasodilation. In addition, LPC suppresses acetylcholine (Ach)-induced responses. We aimed to determine the influence of LPC and LPI on hyperpolarizing responses in vitro and in situ endothelial cells (EC) and identify the underlying mechanisms. Using patch-clamp method, we show that LPI and LPC inhibit EC hyperpolarization to histamine and suppress Na/Ca exchanged (NCX) currents in a concentration-dependent manner. The inhibition is non-mode-specific and unaffected by intracellular GDPβS infusion and tempol, a superoxide dismutase mimetic. In excised mouse aorta, LPI strongly inhibits the sustained and the peak endothelial hyperpolarization induced by Ach, but not by SKA-31, an opener of Ca-dependent K channels of intermediate and small conductance. The hyperpolarizing responses to consecutive histamine applications are strongly reduced by NCX inhibition. In a Ca-re-addition protocol, bepridil, a NCX inhibitor, and KB-R7943, a blocker of reversed NCX, inhibit the hyperpolarizing responses to Ca-re-addition following Ca stores depletion. These finding indicate that LPC and LPI inhibit endothelial hyperpolarization to Ach and histamine independently of G-protein coupled receptors and superoxide anions. Reversed NCX is critical for ER Ca refilling in EC. The inhibition of NCX by LPI and LPC underlies diminished endothelium-dependent responses and endothelial dysfunction accompanied by increased levels of these lipids in the blood.

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Section: Discussionsupporting

confidence: 79%

GPR55 agonist lysophosphatidylinositol and lysophosphatidylcholine inhibit endothelial cell hyperpolarization via GPR-independent suppression of Na+-Ca2+ exchanger and endoplasmic reticulum Ca2+ refilling

Bondarenko

Montecucco

Panasiuk

et al. 2017

Vascular Pharmacology

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“…Mesenteric artery rings from model animals showed weakened endothelium-dependent vasodilator response to acetylcholine in arteries stimulated by phenylephrine compared with control mesenteric artery rings 23 . Mesenteric artery rings from blood stasis treated animals showed reduced endothelium-dependent vasodilator responses to acetylcholine in artery rings stimulated by phenylephrine compared to control aortic rings ACh-mediated vessel relaxation was significantly improved in β-BA (100 mg/kg/d) and β-BA (200 mg/kg/d) groups compared with blood stasis rats ( Fig.…”

Section: Resultsmentioning

confidence: 79%

Pretreatment with β-Boswellic Acid Improves Blood Stasis Induced Endothelial Dysfunction: Role of eNOS Activation

Wang

Chen

Ding

et al. 2015

Sci Rep

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Vascular endothelial cells play an important role in modulating anti-thrombus and maintaining the natural function of vascular by secreting many active substances. β-boswellic acid (β-BA) is an active triterpenoid compound from the extract of boswellia serrate. In this study, it is demonstrated that β-BA ameliorates plasma coagulation parameters, protects endothelium from blood stasis induced injury and prevents blood stasis induced impairment of endothelium-dependent vasodilatation. Moreover, it is found that β-BA significantly increases nitric oxide (NO) and cyclic guanosine 3’, 5’-monophosphate (cGMP) levels in carotid aortas of blood stasis rats. To stimulate blood stasis-like conditions in vitro, human umbilical vein endothelial cells (HUVECs) were exposed to transient oxygen and glucose deprivation (OGD). Treatment of β-BA significantly increased intracellular NO level. Western blot and immunofluorescence as well as immunohistochemistry reveal that β-BA increases phosphorylation of enzyme nitric oxide synthase (eNOS) at Ser1177. In addition, β-BA mediated endothelium-dependent vasodilatation can be markedly blocked by eNOS inhibitor L-NAME in blood stasis rats. In OGD treated HUEVCs, the protective effect of β-BA is attenuated by knockdown of eNOS. In conclusion, the above findings provide convincing evidence for the protective effects of β-BA on blood stasis induced endothelial dysfunction by eNOS signaling pathway.

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“…Previously, by using an in vitro organ culture model, we demonstrated the upregulation of ET B2 expression in VSMC through the activation of the nuclear factor- κ B (NF- κ B) pathway after exposure of the arteries to tumor necrosis factor- α (TNF- α ), a key proinflammatory cytokine [5]. Additionally, during organ culture, expressions of ET A and ET B2 were enhanced by lipid-soluble smoking particles [6, 7] and low-density lipoprotein (LDL) [8]. The above data, to some aspect, indicated a link between upregulation of ETRs and inflammation associated with cardiovascular risk factors.…”

Section: Introductionmentioning

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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Apolipoprotein B of low-density lipoprotein impairs nitric oxide-mediated endothelium-dependent relaxation in rat mesenteric arteries

Cited by 13 publications

References 36 publications

GPR55 agonist lysophosphatidylinositol and lysophosphatidylcholine inhibit endothelial cell hyperpolarization via GPR-independent suppression of Na+-Ca2+ exchanger and endoplasmic reticulum Ca2+ refilling

GPR55 agonist lysophosphatidylinositol and lysophosphatidylcholine inhibit endothelial cell hyperpolarization via GPR-independent suppression of Na+-Ca2+ exchanger and endoplasmic reticulum Ca2+ refilling

Pretreatment with β-Boswellic Acid Improves Blood Stasis Induced Endothelial Dysfunction: Role of eNOS Activation

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

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