ArticleJournal of neuroinflammation2015
Amyloid β peptide-induced inhibition of endothelial nitric oxide production involves oxidative stress-mediated constitutive eNOS/HSP90 interaction and disruption of agonist-mediated Akt activation.
Article in Journal of neuroinflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- The causative role of amyloidosis in the cardiac complications of Alzheimer's disease: a comprehensive systematic review.The Journal of physiology · 2026Pooled it
- Beyond Inhibition: Rebalancing the Hsp90 Chaperone Network as a Therapeutic Strategy for Alzheimer's Disease.Drug design, development and therapy · 2026Review
- Role of Glycolysis and Nitric Oxide Pathway Crosstalk in Macrophages in Atherosclerosis.Current medicinal chemistry · 2026Review
- Circulating amyloid beta 1-40 peptide as an associate of renal function decline.European journal of clinical investigation · 2025Article
- The Correlation of Serum Adropin with Cardiovascular Risk Factors in the Experimental Rat Model of Chronic Kidney Disease and Its Implication in the Ameliorative Effect of Angiotensin-Converting Enzyme Inhibitors.Iranian journal of medical sciences · 2024Article
- Protective effect of long-chain polyunsaturated fatty acids on hepatorenal syndrome in rats.World journal of nephrology · 2024Article
- Cerebrovascular Endothelial Dysfunction: Role of BACE1.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Current biomarkers and treatment strategies in Alzheimer disease: An overview and future perspectives.IBRO neuroscience reports · 2024Review
- Effects of Amyloid Beta (Aβ) Oligomers on Blood-Brain Barrier Using a 3D Microfluidic Vasculature-on-a-Chip Model.Applied sciences (Basel, Switzerland) · 2024Article
- The contribution of β-amyloid, Tau and α-synuclein to blood-brain barrier damage in neurodegenerative disorders.Acta neuropathologica · 2024Review
- The Impact of LY487379 or CDPPB on eNOS Expression in the Mouse Brain and the Effect of Joint Administration of Compounds with NOMolecules (Basel, Switzerland) · 2024Article
- Immune Function of Endothelial Cells: Evolutionary Aspects, Molecular Biology and Role in Atherogenesis.International journal of molecular sciences · 2022Review
- Autonomous regulation of retinal insulin biosynthesis in diabetes.Neuropeptides · 2022Article
- Effects of cerebral amyloid angiopathy on the brain vasculome.Aging cell · 2022Article
- Involvement of Fatty Acids and Their Metabolites in the Development of Inflammation in Atherosclerosis.International journal of molecular sciences · 2022Review
- Amyloid-β 25-35 Induces Neurotoxicity through the Up-Regulation of Astrocytic System XAntioxidants (Basel, Switzerland) · 2021Article
- Alzheimer's Aβ assembly binds sodium pump and blocks endothelial NOS activity via ROS-PKC pathway in brain vascular endothelial cells.iScience · 2021Article
- The Effect ofInternational journal of molecular sciences · 2021Article
- Deficiency of Endothelial Nitric Oxide Synthase (eNOS) Exacerbates Brain Damage and Cognitive Deficit in A Mouse Model of Vascular Dementia.Aging and disease · 2021Article
- Oxidative Stress Triggers Defective Autophagy in Endothelial Cells: Role in Atherothrombosis Development.Antioxidants (Basel, Switzerland) · 2021Review
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Authors and funding
11 authors at 7 institutions in 2 countries.
Funding
Abstract
backgroundAmyloid β (Aβ)-induced vascular dysfunction significantly contributes to the pathogenesis of Alzheimer's disease (AD). Aβ is known to impair endothelial nitric oxide synthase (eNOS) activity, thus inhibiting endothelial nitric oxide production (NO).
methodIn this study, we investigated Aβ-effects on heat shock protein 90 (HSP90) interaction with eNOS and Akt in cultured vascular endothelial cells and also explored the role of oxidative stress in this process.
resultsTreatments of endothelial cells (EC) with Aβ promoted the constitutive association of HSP90 with eNOS but abrogated agonist (vascular endothelial growth factor (VEGF))-mediated HSP90 interaction with Akt. This effect resulted in blockade of agonist-mediated phosphorylation of Akt and eNOS at serine 1179. Furthermore, Aβ stimulated the production of reactive oxygen species in endothelial cells and concomitant treatments of the cells with the antioxidant N-acetyl-cysteine (NAC) prevented Aβ effects in promoting HSP90/eNOS interaction and rescued agonist-mediated Akt and eNOS phosphorylation.
conclusionsThe obtained data support the hypothesis that oxidative damage caused by Aβ results in altered interaction of HSP90 with Akt and eNOS, therefore promoting vascular dysfunction. This mechanism, by contributing to Aβ-mediated blockade of nitric oxide production, may significantly contribute to the cognitive impairment seen in AD patients.
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