ArticleMolecular neurobiology2016
Activation of Transient Receptor Potential Vanilloid 4 is Involved in Neuronal Injury in Middle Cerebral Artery Occlusion in Mice.
Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 90 citations in OpenAlex.
- TRPV4 is involved in NLRP3 and NLRP1 inflammasomes activation after pilocarpine-induced status epilepticus in mice : Concise title: TRPV4-mediated inflammasome activation in epilepsy.Cellular and molecular life sciences : CMLS · 2026Article
- The role of TRPV4 in ischemic stroke.Molecular brain · 2026Review
- An Integrated Analysis of Transcriptomics and Metabolomics Elucidates the Role and Mechanism of TRPV4 in Blunt Cardiac Injury.Metabolites · 2025Article
- The role of TRPV4 in acute sleep deprivation-induced memory impairment: Mechanisms of calcium dysregulation and synaptic plasticity disruption.Cell insight · 2025Article
- Transient receptor potential vanilloid 4 blockage attenuates pyroptosis in hippocampus of mice following pilocarpine‑induced status epilepticus.Acta neuropathologica communications · 2025Article
- Very Low-Intensity Ultrasound Facilitates Glymphatic Influx and Clearance via Modulation of the TRPV4-AQP4 Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- TRPV4 and chloride channels mediate volume sensing in trabecular meshwork cells.American journal of physiology. Cell physiology · 2024Article
- Inflammation-induced TRPV4 channels exacerbate blood-brain barrier dysfunction in multiple sclerosis.Journal of neuroinflammation · 2024Article
- The Multifaceted Functions of TRPV4 and Calcium Oscillations in Tissue Repair.International journal of molecular sciences · 2024Review
- The deletion of AQP4 and TRPV4 affects astrocyte swelling/volume recovery in response to ischemia-mimicking pathologies.Frontiers in cellular neuroscience · 2024Article
- Astrocytic TRPV4 Channels and Their Role in Brain Ischemia.International journal of molecular sciences · 2023Review
- Blockage of TRPV4 Downregulates the Nuclear Factor-Kappa B Signaling Pathway to Inhibit Inflammatory Responses and Neuronal Death in Mice with Pilocarpine-Induced Status Epilepticus.Cellular and molecular neurobiology · 2023Article
- Transient receptor potential ion channels and cerebral stroke.Brain and behavior · 2023Review
- Amantadine Attenuated Hypoxia-Induced Mitochondrial Oxidative Neurotoxicity, Apoptosis, and Inflammation via the Inhibition of TRPM2 and TRPV4 Channels.Molecular neurobiology · 2022Article
- TRPV4: A trigger of pathological RhoA activation in neurological disease.BioEssays : news and reviews in molecular, cellular and developmental biology · 2022Article
- Inhibition of Trpv4 rescues circuit and social deficits unmasked by acute inflammatory response in a Shank3 mouse model of Autism.Molecular psychiatry · 2022Article
- Inhibition of Transient Receptor Potential Vanilloid 4 (TRPV4) Mitigates Seizures.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Article
- A novel antagonist of TRPM2 and TRPV4 channels: Carvacrol.Metabolic brain disease · 2022Article
- TRPV4 contributes to ER stress and inflammation: implications for Parkinson's disease.Journal of neuroinflammation · 2022Article
- CSF Secretion Is Not Altered by NKCC1 Nor TRPV4 Antagonism in Healthy Rats.Brain sciences · 2021Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transient receptor potential vanilloid 4 (TRPV4) is widely expressed in the central nervous system and can be activated by multiple stimuli during cerebral ischemia. Recently, we reported that intracerebroventricular (icv.) injection of HC-067047, a specific TRPV4 antagonist, reduced brain infarction following 60-min of middle cerebral artery occlusion (MCAO). This study was undertaken to investigate the molecular mechanisms underlying TRPV4-mediated neuronal injury in cerebral ischemia. We demonstrated that TRPV4 expression was upregulated in the ipsilateral hippocampus at 4 to 48 h post-MCAO, peaking at 18 h post-MCAO. Treatment with TRPV4 antagonists (HC-067047 and ruthenium red) dose-dependently reduced brain infarction at 24 h post-MCAO. Phosphorylation of protein kinase B (p-Akt) was downregulated and that of extracellular signal-related kinase (p-ERK) was upregulated at 8 to 24 h post-MCAO, which was markedly blocked by treatment with HC-067047. Icv. injection of GSK1016790A (a TRPV4 agonist), dose-dependently induced hippocampal neuronal death, accompanied by an increase in phosphorylation of the NR2B subunit of the N-methyl-D-aspartate receptor (NMDAR). In addition, the level of p-Akt was decreased and that of p-ERK was increased by GSK1016790A-injection, which was sensitive to an NR2B antagonist. The neuronal toxicity of GSK1016790A was blocked by treatment with an NR2B antagonist and a phosphatidylinositol-3-kinase (PI3K) agonist but not by administration of a MAPK/ERK kinase antagonist. We conclude that the activation of TRPV4 is upregulated and involved in neuronal injury during cerebral ischemia and that the neurotoxicity associated with TRPV4-activation is mediated through NR2B-NMDAR and the related downregulation of the Akt signaling pathway.
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