ArticleJournal of neuroinflammation2019
TRPV1 translocated to astrocytic membrane to promote migration and inflammatory infiltration thus promotes epilepsy after hypoxic ischemia in immature brain.
Article in Journal of neuroinflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 53 citations in OpenAlex.
- Prednisone Exposure During Pregnancy Increases Susceptibility to Epilepsy in Adult Offspring Mice.Neurochemical research · 2026Article
- α7nAChR alleviates cognitive impairment by promoting autophagy in astrocytes via CaMKK2/AMPK/mTOR pathway in sepsis-associated encephalopathy.Frontiers in immunology · 2026Article
- Transient Receptor Potential Channels as Key Regulators of Neuroinflammation in Neurological Disorders: Mechanistic Insights, Therapeutic Potentials, and Future Directions.CNS neuroscience & therapeutics · 2025Review
- Cell-specific Nav1.6 knockdown reduced astrocyte-derived Aβ by reverse NaJournal of advanced research · 2025Article
- The Role of Neuroinflammation and Network Anomalies in Drug-Resistant Epilepsy.Neuroscience bulletin · 2025Review
- MUC1‑ND interacts with TRPV1 to promote corneal epithelial cell proliferation in diabetic dry eye mice by partly activating the AKT signaling pathway.Molecular medicine reports · 2024Article
- Dual Role of TRPV1 Channels in Cerebral Stroke: An Exploration from a Mechanistic and Therapeutic Perspective.Molecular neurobiology · 2024Review
- Human TRPV1 is an efficient thermogenetic actuator for chronic neuromodulation.Cellular and molecular life sciences : CMLS · 2024Article
- TRPA1, TRPV1, and Caffeine: Pain and Analgesia.International journal of molecular sciences · 2024Review
- Desflurane improves electrical activity of neurons and alleviates oxygen-glucose deprivation-induced neuronal injury by activating the Kcna1-dependent Kv1.1 channel.Experimental brain research · 2024Article
- Article
- L-F001, a multifunctional fasudil-lipoic acid dimer, antagonizes hypoxic-ischemic brain damage by inhibiting the TLR4/MyD88 signaling pathway.Brain and behavior · 2023Article
- Review
- AQP4 Aggravates Cognitive Impairment in Sepsis-Associated Encephalopathy through Inhibiting NaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Etanercept ameliorates psoriasis progression through regulating high mobility group box 1 pathway.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2023Article
- Anesthesia and analgesia for experimental craniotomy in mice and rats: a systematic scoping review comparing the years 2009 and 2019.Frontiers in neuroscience · 2023Article
- Pre- and Post-Endurance Training Mitigates the Rat Pilocarpine-Induced Status Epilepticus and Epileptogenesis-Associated Deleterious Consequences.International journal of molecular sciences · 2022Article
- Improved gliotransmission by increasing intracellular CaJournal of nanobiotechnology · 2022Article
- Article
- Neuroinflammation and Proinflammatory Cytokines in Epileptogenesis.Molecular neurobiology · 2022Review
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
backgroundNeonatal hypoxic-ischemic brain damage (HIBD), a leading cause of neonatal mortality, has intractable sequela such as epilepsy that seriously affected the life quality of HIBD survivors. We have previously shown that ion channel dysfunction in the central nervous system played an important role in the process of HIBD-induced epilepsy. Therefore, we continued to validate the underlying mechanisms of TRPV1 as a potential target for epilepsy.
methodsNeonatal hypoxic ischemia and oxygen-glucose deprivation (OGD) were used to simulate HIBD in vivo and in vitro. Primarily cultured astrocytes were used to assess the expression of TRPV1, glial fibrillary acidic protein (GFAP), cytoskeletal rearrangement, and inflammatory cytokines by using Western blot, q-PCR, and immunofluorescence. Furthermore, brain electrical activity in freely moving mice was recorded by electroencephalography (EEG). TRPV1 current and neuronal excitability were detected by whole-cell patch clamp.
resultsAstrocytic TRPV1 translocated to the membrane after OGD. Mechanistically, astrocytic TRPV1 activation increased the inflow of Ca
conclusionsCollectively, TRPV1 promoted astrocyte migration thus helped the infiltration of pro-inflammatory cytokines (TNF, IL-1β, IL-6, and iNOS) from astrocytes into the vicinity of neurons to promote epilepsy. Our study provides a strong rationale for astrocytic TRPV1 to be a therapeutic target for anti-epileptogenesis after HIBD.
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Registered trials
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