ArticleBritish journal of pharmacology2010
Acute activation of eNOS by statins involves scavenger receptor-B1, G protein subunit Gi, phospholipase C and calcium influx.
Article in British journal of pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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
19 citing papers in PubMed, 33 citations in OpenAlex.
- The pleiotropic effects of statins: a comprehensive exploration of neurovascular unit modulation and blood-brain barrier protection.Molecular medicine (Cambridge, Mass.) · 2024Review
- SARS-CoV-2 induced HDL dysfunction may affect the host's response to and recovery from COVID-19.Immunity, inflammation and disease · 2023Review
- Phenotypical and Functional Alteration of γδ T Lymphocytes in COVID-19 Patients: Reversal by Statins.Cells · 2022Article
- Off-Target Effect of Lovastatin Disrupts Dietary Lipid Uptake and Dissemination through Pro-Drug Inhibition of the Mesenteric Lymphatic Smooth Muscle Cell Contractile Apparatus.International journal of molecular sciences · 2021Article
- Pleiotropic use of Statins as non-lipid-lowering drugs.International journal of biological sciences · 2020Review
- Pravastatin induces NO synthesis by enhancing microsomal arginine uptake in healthy and preeclamptic placentas.BMC pregnancy and childbirth · 2019Article
- Kang Le Xin Reduces Blood Pressure Through Inducing Endothelial-Dependent Vasodilation by Activating the AMPK-eNOS Pathway.Frontiers in pharmacology · 2019Article
- Article
- Vascular endothelium - Gatekeeper of vessel health.Atherosclerosis · 2016Review
- Xanthine-based KMUP-1 improves HDL via PPARγ/SR-B1, LDL via LDLRs, and HSL via PKA/PKG for hepatic fat loss.Journal of lipid research · 2015Article
- Chronic β1-adrenergic blockade enhances myocardial β3-adrenergic coupling with nitric oxide-cGMP signaling in a canine model of chronic volume overload: new insight into mechanisms of cardiac benefit with selective β1-blocker therapy.Basic research in cardiology · 2015Article
- Effect of rosuvastatin on hyperuricemic rats and the protective effect on endothelial dysfunction.Experimental and therapeutic medicine · 2014Article
- Endothelial dysfunction: the role of sterol regulatory element-binding protein-induced NOD-like receptor family pyrin domain-containing protein 3 inflammasome in atherosclerosis.Current opinion in lipidology · 2014Review
- Effect of pravastatin on echocardiographic circulation parameters in dogs.The Journal of veterinary medical science · 2014Article
- Effect of combined mulberry leaf and fruit extract on liver and skin cholesterol transporters in high fat diet-induced obese mice.Nutrition research and practice · 2014Article
- Regulation of cardiac nitric oxide signaling by nuclear β-adrenergic and endothelin receptors.Journal of molecular and cellular cardiology · 2013Article
- HDL and endothelial protection.British journal of pharmacology · 2013Review
- Niacin: another look at an underutilized lipid-lowering medication.Nature reviews. Endocrinology · 2012Review
- Current therapeutic strategies to mitigate the eNOS dysfunction in ischaemic stroke.Cellular and molecular neurobiology · 2012Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
background and purposeStatins (HMG CoA reductase inhibitors) have beneficial effects independent of reducing cholesterol synthesis and this includes their ability to acutely activate endothelial nitric oxide synthase (eNOS). The mechanism by which this occurs is largely unknown and thus we characterized the pathways by which statins activate NOS, including involvement of scavenger receptor-B1 (SR-B1), which is expressed in endothelial cells and maintains cholesterol concentrations. EXPERIMENTAL APPROACH: Nitric oxide production was monitored in bovine aortic endothelial cells (BAECs) exposed to lovastatin (LOV) or pravastatin (PRA) for 10-20 min, alone or following pre-exposure to the end product of HMG-CoA reductase (mevalonate), G protein inhibitors (pertussis/cholera toxins), phospholipase C (PLC) inhibitor (U-73122), or intracellular and extracellular calcium chelators - BAPTA-AM and EGTA (respectively), or a function blocking antibody to SR-B1. KEY
resultsBoth statins increased NO production in a rapid, dose-dependent and HMG-CoA reductase-independent manner. Inhibiting Gi protein or PLC almost completely blocked statin-induced NO generation. Additionally, removing extracellular calcium inhibited statin-induced NO production. COS-7 cells co-transfected with eNOS and SR-B1 increased NO production when exposed to LOV or high-density lipoprotein (HDL), an agonist of SR-B1. These effects were not observed in COS-7 cells with eNOS alone or co-transfected with bradykinin receptor 2, indicating specificity for SR-B1. Further, pretreatment of BAEC with blocking antibody for SR-B1 blocked NO responses to statins and HDL. CONCLUSIONS AND IMPLICATIONS: LOV and PRA acutely activate eNOS through pathways that include the cell surface receptor SR-B1, Gi protein, phosholipase C and entry of extracellular calcium into endothelial cells.
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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.