ArticleMolecular neurodegeneration2016
Heparan sulfate proteoglycans mediate Aβ-induced oxidative stress and hypercontractility in cultured vascular smooth muscle cells.
Article in Molecular neurodegeneration, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- Heparan Sulfates Regulate Vascular Reactivity in Syndecan 1 Knockout Mice.International journal of molecular sciences · 2026Article
- GDF15 predisposes aortic dissection through regulation of vascular smooth muscle cell proliferation and phenotypic change via the ERK/Akt pathway.American journal of translational research · 2026Article
- Amyloid β alters vascular CaThe Journal of physiology · 2025Article
- AβInternational journal of molecular sciences · 2025Article
- Heparanase inhibitor OGT 2115 induces prostate cancer cell apoptosis via the downregulation of MCL‑1.Oncology letters · 2024Article
- Upregulation of extracellular proteins in a mouse model of Alzheimer's disease.Scientific reports · 2023Article
- Microglia-Mediated Neurovascular Unit Dysfunction in Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2023Review
- Ginsenoside ompound K reduces neuronal damage and improves neuronal synaptic dysfunction by targeting Aβ.Frontiers in pharmacology · 2023Article
- A Preliminary Study on the Relationship between Serum Heparan Sulfate and Cancer-Related Cognitive Impairment: The Moderating Role of Oxidative Stress in Patients with Colorectal Cancer.Current oncology (Toronto, Ont.) · 2022Article
- STAT3 inhibitor mitigates cerebral amyloid angiopathy and parenchymal amyloid plaques while improving cognitive functions and brain networks.Acta neuropathologica communications · 2021Article
- Hypoxia reduces cell attachment of SARS-CoV-2 spike protein by modulating the expression of ACE2, neuropilin-1, syndecan-1 and cellular heparan sulfate.Emerging microbes & infections · 2021Article
- Role of the Extracellular Matrix in Alzheimer's Disease.Frontiers in aging neuroscience · 2021Review
- SIRT1 mediates hypoxic preconditioning induced attenuation of neurovascular dysfunction following subarachnoid hemorrhage.Experimental neurology · 2020Article
- Association of Cigarette Smoking With Cerebrospinal Fluid Biomarkers of Neurodegeneration, Neuroinflammation, and Oxidation.JAMA network open · 2020Article
- Partial loss of endothelial nitric oxide leads to increased cerebrovascular beta amyloid.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020Article
- Neuroprotective Activities of Heparin, Heparinase III, and Hyaluronic Acid on the AACS biomaterials science & engineering · 2018Article
- Modeling Neurodegenerative Microenvironment Using Cortical Organoids Derived from Human Stem Cells.Tissue engineering. Part A · 2018Article
- Apolipoprotein E, Receptors, and Modulation of Alzheimer's Disease.Biological psychiatry · 2018Review
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundSubstantial evidence suggests that amyloid-β (Aβ) species induce oxidative stress and cerebrovascular (CV) dysfunction in Alzheimer's disease (AD), potentially contributing to the progressive dementia of this disease. The upstream molecular pathways governing this process, however, are poorly understood. In this report, we examine the role of heparan sulfate proteoglycans (HSPG) in Aβ-induced vascular smooth muscle cell (VSMC) dysfunction in vitro.
resultsOur results demonstrate that pharmacological depletion of HSPG (by enzymatic degradation with active, but not heat-inactivated, heparinase) in primary human cerebral and transformed rat VSMC mitigates Aβ(1-40⁻) and Aβ(1-42⁻)induced oxidative stress. This inhibitory effect is specific for HSPG depletion and does not occur with pharmacological depletion of other glycosaminoglycan (GAG) family members. We also found that Aβ(1-40) (but not Aβ(1-42)) causes a hypercontractile phenotype in transformed rat cerebral VSMC that likely results from a HSPG-mediated augmentation in intracellular Ca(2+) activity, as both Aβ(1-40⁻)induced VSMC hypercontractility and increased Ca(2+) influx are inhibited by pharmacological HSPG depletion. Moreover, chelation of extracellular Ca(2+) with ethylene glycol tetraacetic acid (EGTA) does not prevent the production of Aβ(1-40⁻) or Aβ(1-42⁻)mediated reactive oxygen species (ROS), suggesting that Aβ-induced ROS and VSMC hypercontractility occur through different molecular pathways.
conclusionsTaken together, our data indicate that HSPG are critical mediators of Aβ-induced oxidative stress and Aβ(1-40⁻)induced VSMC dysfunction.
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