ArticleFrontiers in molecular neuroscience2018
Inhibition of Heat Shock Protein 90 by 17-AAG Reduces Inflammation via P2X7 Receptor/NLRP3 Inflammasome Pathway and Increases Neurogenesis After Subarachnoid Hemorrhage in Mice.
Article in Frontiers in molecular neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 54 citations in OpenAlex.
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- Retinal Pigment Epithelium Under Oxidative Stress: Chaperoning Autophagy and Beyond.International journal of molecular sciences · 2025Review
- Targeting the P2X7 receptor in cerebrovascular diseases: from molecular mechanisms to preclinical therapeutic potential.Frontiers in pharmacology · 2025Review
- Activation of Piezo1 by intracranial hypertension induced neuronal apoptosis via activating hippo pathway.CNS neuroscience & therapeutics · 2024Article
- MFGE8 promotes adult hippocampal neurogenesis in rats following experimental subarachnoid hemorrhage via modifying the integrin β3/Akt signaling pathway.Cell death discovery · 2024Article
- HSP90, a Common Therapeutic Target for Suppressing Skin Injury Caused by Exposure to Chemically Diverse Classes of Blistering Agents.The Journal of pharmacology and experimental therapeutics · 2024Article
- Anti-inflammatory activities of novel heat shock protein 90 isoform selective inhibitors in BV-2 microglial cells.Frontiers in molecular biosciences · 2024Article
- P2X7 receptor antagonist A-438079 alleviates oxidative stress of lung in LPS-induced septic rats.Purinergic signalling · 2023Article
- The NLRP3 inflammasome: role in the pathobiology of chronic pain.Inflammopharmacology · 2023Review
- NLRP3 Inflammasome Overactivation in Patients with Aneurysmal Subarachnoid Hemorrhage.Translational stroke research · 2023Article
- The Potential of NLRP3 Inflammasome as a Therapeutic Target in Neurological Diseases.Molecular neurobiology · 2023Review
- The NLRP3 inflammasome is involved in resident intruder paradigm-induced aggressive behaviors in mice.Frontiers in pharmacology · 2023Article
- The Inflammasome NLR Family Pyrin Domain-Containing Protein 3 (NLRP3) as a Novel Therapeutic Target for Idiopathic Pulmonary Fibrosis.The American journal of pathology · 2022Review
- Knock-Down of CD24 in Astrocytes Aggravates Oxyhemoglobin-Induced Hippocampal Neuron Impairment.Neurochemical research · 2022Article
- Hypoxia Tolerant Species: The Wisdom of Nature Translated into Targets for Stroke Therapy.International journal of molecular sciences · 2021Review
- MFGE8 mitigates brain injury in a rat model of SAH by maintaining vascular endothelial integrity via TIGβ5/PI3K/CXCL12 signaling.Experimental brain research · 2021Article
- Differential Expression of Inflammasome-Related Genes in Induced Pluripotent Stem-Cell-Derived Retinal Pigment Epithelial Cells with or without History of Age-Related Macular Degeneration.International journal of molecular sciences · 2021Article
- TAS-116, a Well-Tolerated Hsp90 Inhibitor, Prevents the Activation of the NLRP3 Inflammasome in Human Retinal Pigment Epithelial Cells.International journal of molecular sciences · 2021Article
- The Potential Role of Inflammation in Modulating Endogenous Hippocampal Neurogenesis After Spinal Cord Injury.Frontiers in neuroscience · 2021Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Subarachnoid hemorrhage (SAH) is a life-threatening cerebrovascular disease that usually has a poor prognosis. Heat shock proteins (HSPs) have been implicated in the mechanisms of SAH-associated damage, including increased inflammation and reduced neurogenesis. The aim of this study was to investigate the effects of HSP90 inhibition on inflammation and neurogenesis in a mouse model of experimental SAH induced by endovascular surgery. Western blotting showed HSP90 levels to be decreased, while neurogenesis, evaluated by 5-bromo-2'-deoxyuridine (BrdU) immunohistochemistry, was decreased in the hippocampuses of SAH mice. SAH also induced pro-inflammatory factors such as interleukin-1β (IL-1β), capase-1 and the NLRP3 inflammasome. However, intraperitoneal administration of the specific HSP90 inhibitor 17-allylamino-17-demethoxygeldanamycin (17-AAG) reduced the levels of HSP90, NLRP3, ASC, caspase-1 and IL-1β, while increasing the levels of brain-derived neurotrophic factor and doublecortin (DCX), as well as the number of BrdU-positive cells in SAH mice. In addition, 17-AGG improved short- and long-term neurobehavioral outcomes. The neuroprotective and anti-inflammatory effects of 17-AGG were reversed by recombinant HSP90 (rHSP90); this detrimental effect of HSP90 was inhibited by the specific P2X7 receptor (P2X7R) inhibitor A438079, indicating that SAH-induced inflammation and inhibition of neurogenesis were likely mediated by HSP90 and the P2X7R/NLRP3 inflammasome pathway. HSP90 inhibition by 17-AAG may be a promising therapeutic strategy for the treatment of SAH.
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