ArticleFrontiers in aging neuroscience2013
Thrombin, a mediator of cerebrovascular inflammation in AD and hypoxia.
Article in Frontiers in aging neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 100 citations in OpenAlex.
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- Association between susceptibility value and cerebral blood flow in the bilateral putamen in patients undergoing hemodialysis.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Article
- Fibrin-Targeting Immunotherapy for Dementia.The journal of prevention of Alzheimer's disease · 2023Article
- Cellular mechanisms of fibrin (ogen): insight from neurodegenerative diseases.Frontiers in neuroscience · 2023Review
- Direct Oral Anticoagulants (DOACs) for Therapeutic Targeting of Thrombin, a Key Mediator of Cerebrovascular and Neuronal Dysfunction in Alzheimer's Disease.Biomedicines · 2022Review
- Key brain cell interactions and contributions to the pathogenesis of Alzheimer's disease.Frontiers in cell and developmental biology · 2022Review
- Review
- Distinct brain regional proteome changes in the rTg-DI rat model of cerebral amyloid angiopathy.Journal of neurochemistry · 2021Article
- Thrombin aggravates hypoxia/reoxygenation injury of astrocytes by activating the autophagy pathway mediated by SPRED2.Experimental and therapeutic medicine · 2021Article
- Dabigatran mitigates cisplatin-mediated nephrotoxicity through down regulation of thrombin pathway.Journal of advanced research · 2021Article
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Authors and funding
6 authors at 2 institutions in 1 country.
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Abstract
Considerable evidence implicates hypoxia and vascular inflammation in Alzheimer's disease (AD). Thrombin, a multifunctional inflammatory mediator, is demonstrable in the brains of AD patients both in the vessel walls and senile plaques. Hypoxia-inducible factor 1α (HIF-1α), a key regulator of the cellular response to hypoxia, is also upregulated in the vasculature of human AD brains. The objective of this study is to investigate inflammatory protein expression in the cerebrovasculature of transgenic AD mice and to explore the role of thrombin as a mediator of cerebrovascular inflammation and oxidative stress in AD and in hypoxia-induced changes in brain endothelial cells. Immunofluorescent analysis of the cerebrovasculature in AD mice demonstrates significant (p < 0.01-0.001) increases in thrombin, HIF-1α, interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), matrix metalloproteinases (MMPs), and reactive oxygen species (ROS) compared to controls. Administration of the thrombin inhibitor dabigatran (100 mg/kg) to AD mice for 34 weeks significantly decreases expression of inflammatory proteins and ROS. Exposure of cultured brain endothelial cells to hypoxia for 6 h causes an upregulation of thrombin, HIF-1α, MCP-1, IL-6, and MMP2 and ROS. Treatment of endothelial cells with the dabigatran (1 nM) reduces ROS generation and inflammatory protein expression (p < 0.01-0.001). The data demonstrate that inhibition of thrombin in culture blocks the increase in inflammatory protein expression and ROS generation evoked by hypoxia. Also, administration of dabigatran to transgenic AD mice diminishes ROS levels in brain and reduces cerebrovascular expression of inflammatory proteins. Taken together, these results suggest that inhibiting thrombin generation could have therapeutic value in AD and other disorders where hypoxia, inflammation, and oxidative stress are involved.
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