ArticleJournal of neuropathology and experimental neurology2014
Involvement of matrix metalloproteinase-9 in amyloid-β 1-42-induced shedding of the pericyte proteoglycan NG2.
Article in Journal of neuropathology and experimental neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 45 citations in OpenAlex.
- Proteolytic remodelling of the extracellular matrix by pericytes.The FEBS journal · 2026Review
- Post-mortem evidence of pathogenic angiogenesis and abnormal vascular function in early Alzheimer's disease.Brain : a journal of neurology · 2026Article
- Entwined processes in Alzheimer's disease: Brain cellular senescence and Alzheimer's disease pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Molecular Insights into Bromocriptine Binding to GPCRs Within Histamine-Linked Signaling Networks: Network Pharmacology, Pharmacophore Modeling, and Molecular Dynamics Simulation.International journal of molecular sciences · 2025Article
- Glial Cells in Alzheimer's Disease: Pathogenic Mechanisms and Therapeutic Frontiers.Journal of molecular neuroscience : MN · 2025Review
- Inflammatory aspects of Alzheimer's disease.Acta neuropathologica · 2024Review
- Amyloid β oligomer induces cerebral vasculopathy via pericyte-mediated endothelial dysfunction.Alzheimer's research & therapy · 2024Article
- Nerve-Glial antigen 2: unmasking the enigmatic cellular identity in the central nervous system.Frontiers in immunology · 2024Review
- The Active Role of Pericytes During Neuroinflammation in the Adult Brain.Cellular and molecular neurobiology · 2023Review
- Proteolysis: a key post-translational modification regulating proteoglycans.American journal of physiology. Cell physiology · 2022Review
- Blood-brain barrier leakage in Alzheimer's disease: From discovery to clinical relevance.Pharmacology & therapeutics · 2022Review
- Extracellular Matrix in Neural Plasticity and Regeneration.Cellular and molecular neurobiology · 2022Review
- Neural crest cell-derived pericytes act as pro-angiogenic cells in human neocortex development and gliomas.Fluids and barriers of the CNS · 2021Review
- Neurovascular Alterations in Vascular Dementia: Emphasis on Risk Factors.Frontiers in aging neuroscience · 2021Article
- Apolipoprotein E isoforms differentially regulate matrix metallopeptidase 9 function in Alzheimer's disease.Neurobiology of aging · 2020Article
- Multifaceted roles of pericytes in central nervous system homeostasis and disease.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020Review
- Interactions between Amyloid-Β Proteins and Human Brain Pericytes: Implications for the Pathobiology of Alzheimer's Disease.Journal of clinical medicine · 2020Review
- Amyloid-beta 1-40 is associated with alterations in NG2+ pericyte population ex vivo and in vitro.Aging cell · 2018Article
- Amylin alters human brain pericyte viability and NG2 expression.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017Article
- Deficiency in matrix metalloproteinase-2 results in long-term vascular instability and regression in the injured mouse spinal cord.Experimental neurology · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deposition of amyloid-β (Aβ) 1-42, the major component of senile plaques characteristic of Alzheimer disease, affects brain microvascular integrity and causes blood-brain barrier dysfunction, increased angiogenesis, and pericyte degeneration. To understand the cellular events underlying Aβ1-42 effects on microvascular alterations, we investigated whether different aggregation forms of Aβ1-42 affect shedding of the pericyte proteoglycan NG2 and whether they affect proteolytic cleavage mediated by matrix metalloproteinase (MMP)-9. We found decreased levels of soluble NG2, total MMP-9, and MMP-9 activity in pericyte culture supernatants in response to fibril-enriched preparations of Aβ1-42. Conversely, oligomer-enriched preparations of Aβ1-42 increased soluble NG2 levels in the supernatants. This increase was ablated by the MMP-9/MMP-2 inhibitor SB-3CT. There was also a trend toward increased MMP-9 activity observed after oligomeric Aβ1-42 exposure. Our results, demonstrating an Aβ1-42 aggregation-dependent effect on levels of NG2 and MMP-9, support previous studies showing an impact of Aβ1-42 on vascular integrity and thereby add to our understanding of mechanisms behind the microvascular changes commonly found in patients with Alzheimer disease.
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