ArticleCardiovascular research2017
Amyloidogenic medin induces endothelial dysfunction and vascular inflammation through the receptor for advanced glycation endproducts.
Article in Cardiovascular research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 48 citations in OpenAlex.
- Rapid elongation drives the exceptionally fast aggregation of the most common localized human amyloid medin.Communications chemistry · 2026Article
- Neutrophils and aortic medial amyloid: mutually beneficial or a dangerous combination?Frontiers in immunology · 2026Article
- Aortic Stiffness and Alzheimer's Disease: The Medin Connection.Biomolecules · 2025Review
- Medin induces pro-inflammatory activation of human brain vascular smooth muscle cells.Physiological reports · 2025Article
- Investigating Medin Cleavage Accessibility in MfgE8: Conformational Insights Derived from Molecular Dynamics Simulations and AlphaFold2 Models.bioRxiv : the preprint server for biology · 2024Article
- Proteomics of mouse brain endothelium uncovers dysregulation of vesicular transport pathways during aging.Nature aging · 2024Article
- Transcriptomic analyses reveal proinflammatory activation of human brain microvascular endothelial cells by aging-associated peptide medin and reversal by nanoliposomes.Scientific reports · 2023Article
- Type 1 Diabetes Impairs Endothelium-Dependent Relaxation Via Increasing Endothelial Cell Glycolysis Through Advanced Glycation End Products, PFKFB3, and Nox1-Mediated Mechanisms.Hypertension (Dallas, Tex. : 1979) · 2023Article
- Light, Water, and Melatonin: The Synergistic Regulation of Phase Separation in Dementia.International journal of molecular sciences · 2023Review
- Article
- Vascular smooth muscle cell senescence accelerates medin aggregation via small extracellular vesicle secretion and extracellular matrix reorganization.Aging cell · 2023Article
- Review
- Chronic Cognitive and Cerebrovascular Function after Mild Traumatic Brain Injury in Rats.Journal of neurotrauma · 2022Article
- Inflammatory Role of Milk Fat Globule-Epidermal Growth Factor VIII in Age-Associated Arterial Remodeling.Journal of the American Heart Association · 2022Article
- Pathophysiology of RAGE in inflammatory diseases.Frontiers in immunology · 2022Review
- MFG-E8 (LACTADHERIN): a novel marker associated with cerebral amyloid angiopathy.Acta neuropathologica communications · 2021Article
- Inflammation, Nitro-Oxidative Stress, Impaired Autophagy, and Insulin Resistance as a Mechanistic Convergence Between Arterial Stiffness and Alzheimer's Disease.Frontiers in molecular biosciences · 2021Review
- Medin aggregation causes cerebrovascular dysfunction in aging wild-type mice.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Medin Oligomer Membrane Pore Formation: A Potential Mechanism of Vascular Dysfunction.Biophysical journal · 2020Article
- Endothelial Immune Activation by Medin: Potential Role in Cerebrovascular Disease and Reversal by Monosialoganglioside-Containing Nanoliposomes.Journal of the American Heart Association · 2020Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
aimsMedin is a common amyloidogenic protein in humans that accumulates in arteries with advanced age and has been implicated in vascular degeneration. Medin's effect on endothelial function remains unknown. The aims are to assess medin's effects on human arteriole endothelial function and identify potential mechanisms underlying medin-induced vascular injury. METHODS AND
resultsEx vivo human adipose and leptomeningeal arterioles were exposed (1 h) to medin (0.1, 1, or 5 µM) without or with FPS-ZM1 [100 µM, receptor for advanced glycation endproducts (RAGE)-specific inhibitor] and endothelium-dependent function (acetylcholine dilator response) and endothelium-independent function (dilator response to nitric oxide donor diethylenetriamine NONOate) were compared with baseline control. Human umbilical vein endothelial cells were exposed to medin without or with FPS-ZM1 and oxidative and nitrative stress, cell viability, and pro-inflammatory signaling measures were obtained. Medin caused impaired endothelial function (vs. baseline response: -45.2 ± 5.1 and -35.8 ± 7.9% in adipose and leptomeningeal arterioles, respectively, each P < 0.05). Dilator response to NONOate was not significantly changed. Medin decreased arteriole and endothelial cell nitric oxide production, increased superoxide production, reduced endothelial cell viability, proliferation, and migration. Medin increased gene and protein expression of interleukin-6 and interleukin-8 via activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB). Medin-induced endothelial dysfunction and oxidative stress were reversed by antioxidant polyethylene glycol superoxide dismutase and by RAGE inhibitor FPS-ZM1.
conclusionsMedin causes human microvascular endothelial dysfunction through oxidative and nitrative stress and promotes pro-inflammatory signaling in endothelial cells. These effects appear to be mediated via RAGE. The findings represent a potential novel mechanism of vascular injury.
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Registered trials
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.