ArticleCirculation2001
Regulation of endothelial nitric oxide synthase expression in the vascular wall and in mononuclear cells from hypercholesterolemic rabbits.
Article in Circulation, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 46 citations in OpenAlex.
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- Widespread Coronary Dysfunction in the Absence of HDL Receptor SR-B1 in an Ischemic Cardiomyopathy Mouse Model.Scientific reports · 2017Article
- Time-course changes of nLDL-induced erectile dysfunction.International journal of impotence research · 2017Article
- Post-Transcriptional Regulation of Endothelial Nitric Oxide Synthase Expression by Polypyrimidine Tract-Binding Protein 1.Arteriosclerosis, thrombosis, and vascular biology · 2015Article
- Role for Tetrahydrobiopterin in the Fetoplacental Endothelial Dysfunction in Maternal Supraphysiological Hypercholesterolemia.Oxidative medicine and cellular longevity · 2015Review
- Endothelial dysfunction abrogates the efficacy of normobaric hyperoxia in stroke.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Ceacam1 deletion causes vascular alterations in large vessels.American journal of physiology. Endocrinology and metabolism · 2013Article
- Simvastatin modulates remodeling of Kv4.3 expression in rat hypertrophied cardiomyocytes.International journal of biological sciences · 2012Article
- Fetoplacental vascular endothelial dysfunction as an early phenomenon in the programming of human adult diseases in subjects born from gestational diabetes mellitus or obesity in pregnancy.Experimental diabetes research · 2011Review
- Therapeutic interventions and oxidative stress in diabetes.Frontiers in bioscience (Landmark edition) · 2009Review
- Tumor necrosis factor-alpha downregulates endothelial nitric oxide synthase mRNA stability via translation elongation factor 1-alpha 1.Circulation research · 2008Article
- Alternative polyadenylation sites of human endothelial nitric oxide synthase mRNA.Biochemical and biophysical research communications · 2007Article
- Relative reduction of endothelial nitric-oxide synthase expression and transcription in atherosclerosis-prone regions of the mouse aorta and in an in vitro model of disturbed flow.The American journal of pathology · 2007Article
- Physiological role of ROCKs in the cardiovascular system.American journal of physiology. Cell physiology · 2006Review
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWe recently obtained evidence demonstrating that cultured bovine endothelial cells contain cytosolic proteins that form complexes with the 3'-untranslated region of endothelial nitric oxide synthase (eNOS) mRNA and are associated with its destabilization. The aim of this study was to determine the presence of such proteins and eNOS expression in hypercholesterolemic rabbits as an in vivo model of endothelial dysfunction. METHODS AND
resultsEndothelium-dependent relaxation to acetylcholine and the calcium ionophore A23187 was reduced in aortic segments from hypercholesterolemic rabbits compared with controls. Treatment of hypercholesterolemic rabbits with cerivastatin (0.1 mg. kg body wt(-1). d(-1)) restored endothelium-dependent relaxation. Aortic eNOS expression was reduced in hypercholesterolemic rabbits and was accompanied by enhanced binding activity of a 60-kDa cytosolic protein and reduced stability of eNOS mRNA. Cerivastatin treatment upregulated eNOS expression and reduced the interaction of the cytosolic protein with the 3'-untranslated region of eNOS mRNA. Mononuclear cells from hypercholesterolemic rabbits also showed a marked reduction of eNOS expression and eNOS mRNA stability and an increase in binding activity of the cytosolic protein, which were also prevented by cerivastatin treatment.
conclusionsThese results demonstrate the presence of a 60-kDa protein that binds to eNOS mRNA and reductions in eNOS expression in both vascular wall and mononuclear cells that are prevented by cerivastatin.
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