The eNOS signalosome and its link to endothelial dysfunction

Siragusa, Mauro; Fleming, Ingrid

doi:10.1007/s00424-016-1839-0

Cited by 140 publications

(119 citation statements)

References 123 publications

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“…phosphorylation through Akt1 10, 11 ) and protein-protein interactions [e.g. caveolin-1 (CAV1) 12 or heat shock protein 90 (HSP90) 13 ] and other assorted regulators 14 . NO production is stimulated by various vasoactive factors including catecholamines 15 , bradykinin 16 , and serotonin 17 as well as physical factors such as fluid shear stress 18 .…”

Section: Nitric Oxide (No) and No Sensitive Soluble Guanylate Cyclasementioning

confidence: 99%

Contemporary Approaches to Modulating the Nitric Oxide–cGMP Pathway in Cardiovascular Disease

Kraehling

Sessa

2017

Circulation Research

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Endothelial cells lining the vessel wall control important aspects of vascular homeostasis. In particular, the production of endothelium-derived nitric oxide and activation of soluble guanylate cyclase promotes endothelial quiescence and governs vasomotor function and proportional remodeling of blood vessels. Here, we discuss novel approaches to improve endothelial nitric oxide generation and preserve its bioavailability. We also discuss therapeutic opportunities aimed at activation of soluble guanylate cyclase for multiple cardiovascular indications.

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Section: Nitric Oxide (No) and No Sensitive Soluble Guanylate Cyclasementioning

confidence: 99%

Contemporary Approaches to Modulating the Nitric Oxide–cGMP Pathway in Cardiovascular Disease

Kraehling

Sessa

2017

Circulation Research

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“…The activity of eNOS can be regulated by a number of post-translational modifications. Among them, protein kinase B (Akt) induces eNOS-Ser 1177 phosphorylation to modulate endothelial NO production in response to a wide variety of stimuli1213.…”

mentioning

confidence: 99%

Oleanolic acid ameliorates high glucose-induced endothelial dysfunction via PPARδ activation

Zhang

Jiang

Xie

et al. 2017

Sci Rep

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Oleanolic acid (3β-hydroxyolean-12-en-28-oic acid, OA) is a pentacyclic triterpenes widely distributed in food, medicinal plants and nutritional supplements. OA exhibits various pharmacological properties, such as hepatoprotective and anti-tumor effects. In this study, we analyzed the effect of OA on endothelial dysfunction induced by high glucose in human vascular endothelial cells (ECs). Western blotting showed that OA attenuated high glucose-reduced nitric production oxide (NO) as well as Akt-Ser473 and eNOS-Ser1177 phosphorylation in cultured human umbilical vein ECs (HUVECs). Next, luciferase reporter assay showed that OA activated peroxisome proliferators-activated receptor δ (PPARδ) activity. Quantitative reverse transcriptase PCR (qRT-PCR) demonstrated that OA increased the expressions of PPARδ target genes (PDK4, ADRP and ANGPTL4) in ECs. Meanwhile, the induced expressions of PDK4, ADRP and ANGPTL4 by OA were inhibited by GSK0660, a specific antagonist of PPARδ. In addition, inhibition of PPARδ abolished OA-induced the Akt-Ser473 and eNOS-Ser1177 phosphorylation, and NO production. Finally, by using Multi Myograph System, we showed that OA prevented high glucose-impaired vasodilation. This protective effect on vasodilation was inhibited in aortic rings pretreated with GSK0660. Collectively, we demonstrated that OA improved high glucose-impaired endothelial function via a PPARδ-mediated mechanism and through eNOS/Akt/NO pathway.

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“…Nitric oxide (NO) is a soluble, short-lived and freely diffusible gas, which has been reported to conduct numerous signaling tasks throughout the organism such as the central and peripheral nervous system (3). NO is produced after activation of glutamate receptors, mainly N-methyl-D aspatate (NMDA) subtype.…”

Section: Introductionmentioning

confidence: 99%

eNOS and XRCC4 VNTR variants contribute to formation of nicotine dependence and/or schizophrenia

Pehlıvan¹,

Uysal²,

Aydin³

et al. 2017

BLL

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BACKGROUND: This study aimed to evaluate whether VNTR variants in the Endothelial Nitric Oxide Synthase (eNOS) and the XRCC4 gene play any role in nicotine dependence (ND) and/or Schizophrenia+ND (Sch+ND) ethiopathogenesis. METHODS: Present study included 100 individuals with ND, 60 patients with Sch+ND, and 70 healthy controls. These variants were analyzed using PCR. RESULTS: The cases with ND had higher eNOS VNTR-BB genotype than the healthy control subjects (p = 0.001). eNOS-AA genotype was lower in cases with Sch+ND and ND groups compared to the controls (p = 0.001, p = 0.001, respectively). eNOS-B allele was found signifi cantly more frequently in Sch+ND group compared to the controls (p = 0.001). eNOS-A allele was signifi cantly lower in ND group than the controls (p = 0.001). XRCC4-ID genotype was more common in the ND group than the control group (p = 0.001) as heterozygosity disadvantage. XRCC4-DD genotype was more common in the Sch+ND group compared to the controls (p = 0.035). The frequency of XRCC4-I allele was lower in the Sch+ND group compared to the controls (p = 0.012). CONCLUSIONS: Our results showed that eNOS and XRCC4 VNTR variants might play a potential role in Sch+ND and/or ND pathophysiology (Tab. 2, Ref. 48). Text in PDF www.elis.sk.

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The eNOS signalosome and its link to endothelial dysfunction

Cited by 140 publications

References 123 publications

Contemporary Approaches to Modulating the Nitric Oxide–cGMP Pathway in Cardiovascular Disease

Contemporary Approaches to Modulating the Nitric Oxide–cGMP Pathway in Cardiovascular Disease

Oleanolic acid ameliorates high glucose-induced endothelial dysfunction via PPARδ activation

eNOS and XRCC4 VNTR variants contribute to formation of nicotine dependence and/or schizophrenia

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