Differential effects of HIF-1 inhibition by YC-1 on the overall outcome and blood-brain barrier damage in a rat model of ischemic stroke - Wikidata - wikimedia - TriplyDB

Differential effects of HIF-1 inhibition by YC-1 on the overall outcome and blood-brain barrier damage in a rat model of ischemic stroke

Differential effects of HIF-1 inhibition by YC-1 on the overall outcome and blood-brain barrier damage in a rat model of ischemic stroke

http://www.wikidata.org/entity/Q34081831

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Cerebral hypoxia/ischemia selectively disrupts tight junctions complexes in stem cell-derived human brain microvascular endothelial cells Relative Contribution of Prolyl Hydroxylase-Dependent and -Independent Degradation of HIF-1alpha by Proteasomal Pathways in Cerebral Ischemia.Endothelial progenitor cells transplantation attenuated blood-brain barrier damage after ischemia in diabetic mice via HIF-1α.Fumaric acid esters stimulate astrocytic VEGF expression through HIF-1α and Nrf2.Ischemic tolerance in an in vivo model of glutamate preconditioning.The HIF-1 inhibitor YC-1 decreases reactive astrocyte formation in a rodent ischemia model Redox signaling pathways involved in neuronal ischemic preconditioning Hypoxia-inducible factor 1 is essential for spontaneous recovery from traumatic brain injury and is a key mediator of heat acclimation induced neuroprotection.HIF-1 Mediates Renal Fibrosis in OVE26 Type 1 Diabetic Mice.Chronic cerebral hypoperfusion causes decrease of O-GlcNAcylation, hyperphosphorylation of tau and behavioral deficits in mice.Hypoxia-inducible factor 1 contributes to N-acetylcysteine's protection in stroke.Hypoxia inducible factor-1: its potential role in cerebral ischemia.The novel proteasome inhibitor BSc2118 protects against cerebral ischaemia through HIF1A accumulation and enhanced angioneurogenesis.From chronic cerebral hypoperfusion to Alzheimer-like brain pathology and neurodegeneration.Hypoxia selectively disrupts brain microvascular endothelial tight junction complexes through a hypoxia-inducible factor-1 (HIF-1) dependent mechanism.β2-Adrenergic Receptor-Mediated HIF-1α Upregulation Mediates Blood Brain Barrier Damage in Acute Cerebral Ischemia.Inhibition of HIF prolyl-4-hydroxylases by FG-4497 reduces brain tissue injury and edema formation during ischemic stroke.Optimization of Evans blue quantitation in limited rat tissue samples.Changes in levels of hypoxia-induced mediators in rat hippocampus during chronic cerebral hypoperfusion.Therapeutic window for YC‑1 following glutamate‑induced neuronal damage and transient focal cerebral ischemia.HIF-1α/Beclin1-Mediated Autophagy Is Involved in Neuroprotection Induced by Hypoxic Preconditioning Inhibition of HIF-1α Reduced Blood Brain Barrier Damage by Regulating MMP-2 and VEGF During Acute Cerebral Ischemia

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Differential effects of HIF-1 inhibition by YC-1 on the overall outcome and blood-brain barrier damage in a rat model of ischemic stroke

http://www.wikidata.org/entity/Q34081831

description

2011 nî lūn-bûn

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2011 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած

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2011 թվականի նոյեմբերին հրատարակված գիտական հոդված

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2011年の論文

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Differential effects of HIF-1 ...... a rat model of ischemic stroke

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JOURNAL.PONE.0027798

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Differential effects of HIF-1 ...... a rat model of ischemic stroke

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Bo Zhou

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Honglian Shi

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Jingqi Yan

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Saeid Taheri

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Activation of vascular endothelial growth factor gene transcription by hypoxia-inducible factor 1

Erythropoietin prevents neuronal apoptosis after cerebral ischemia and metabolic stress

Endothelial claudin: claudin-5/TMVCF constitutes tight junction strands in endothelial cells

Targeting HIF-1 for cancer therapy

Protection from oxidative stress-induced apoptosis in cortical neuronal cultures by iron chelators is associated with enhanced DNA binding of hypoxia-inducible factor-1 and ATF-1/CREB and increased expression of glycolytic enzymes, p21(waf1/cip1), a

Tumor cells secrete a vascular permeability factor that promotes accumulation of ascites fluid

[Magnetic resonance tomography in stroke--its methodological bases and clinical use]

Edema and brain trauma.

Hypoxia-induced vascular endothelial growth factor expression causes vascular leakage in the brain.

Estrogen suppresses cardiac IL-6 after trauma-hemorrhage via a hypoxia-inducible factor 1 alpha-mediated pathway.

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scholarly article

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10.1371/JOURNAL.PONE.0027798

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11

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51824301

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22110762

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blood–brain barrier

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3218033

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