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Cited by 149Epilepsy research and treatmentNeuroinflammation and Neurodegeneration MechanismsIon Channels and Receptors

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TRPV4-induced inflammatory response is involved in neuronal death in pilocarpine model of temporal lobe epilepsy in mice

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Wang, Zhouqing, Zhou, Li, An, Dong, Xu, Weixing, Wu, Chunfeng, Sha, Sha, Li, Yingchun, Zhu, Yichao, Chen, Aidong, Du, Yimei, Chen, Lei, Chen, Ling·2019·Cell Death & Disease
DOI 10.1038/s41419-019-1612-3PMC PMC6522539
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Abstract

Activation of transient receptor potential vanilloid 4 (TRPV4) induces neuronal injury. TRPV4 activation enhances inflammatory response and promotes the proinflammatory cytokine release in various types of tissue and cells. Hyperneuroinflammation contributes to neuronal damage in epilepsy. Herein, we examined the contribution of neuroinflammation to TRPV4-induced neurotoxicity and its involvement in the inflammation and neuronal damage in pilocarpine model of temporal lobe epilepsy in mice. Icv. injection of TRPV4 agonist GSK1016790A (GSK1016790A-injected mice) increased ionized calcium binding adapter molecule-1 (Iba-1) and glial fibrillary acidic protein (GFAP) protein levels and Iba-1-positive (Iba-1+) and GFAP-positive (GFAP+) cells in hippocampi, which indicated TRPV4-induced microglial cell and astrocyte activation. The protein levels of nucleotide-binding oligomerization domain-like receptor pyrin domain containing 3 (NLRP3) inflammasome components NLRP3, apoptosis-related spotted protein (ASC) and cysteinyl aspartate-specific protease-1 (caspase-1) were increased in GSK1016790A-injected mice, which indicated NLRP3 inflammasome activation. GSK1016790A also increased proinflammatory cytokine IL-1β, TNF-α and IL-6 protein levels, which were blocked by caspase-1 inhibitor Ac-YVAD-cmk. GSK1016790A-induced neuronal death was attenuated by Ac-YVAD-cmk. Icv. injection of TRPV4-specific antagonist HC-067047 markedly increased the number of surviving cells 3 d post status epilepticus in pilocarpine model of temporal lobe epilepsy in mice (pilocarpine-induced status epilepticus, PISE). HC-067047 also markedly blocked the increase in Iba-1 and GFAP protein levels, as well as Iba-1+ and GFAP+ cells 3 d post-PISE. Finally, the increased protein levels of NLRP3, ASC and caspase-1 as well as IL-1β, TNF-α and IL-6 were markedly blocked by HC-067047. We conclude that TRPV4-induced neuronal death is mediated at least partially by enhancing the neuroinflammatory response, and this action is involved in neuronal injury following status epilepticus.

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Metadata

Authors
Wang, Z., Zhou, L., An, D., Xu, W., Wu, C., Sha, S., Li, Y., Zhu, Y., Chen, A., Du, Y., Chen, L., & Chen, L.
Affiliations
  • Nanjing Medical University (CN)
  • Nanjing Children's Hospital (CN)
  • Wuhan Union Hospital (CN)
Corresponding author
  • Chen, Lei
  • Chen, Ling
ORCID
Venue
Cell Death & Disease
Publisher
Springer Science and Business Media LLC
Published
2019-05-16
Volume
10
Issue
6
Pages
386-386
ISSN
2041-4889 (ISSN-L)
DOI
10.1038/s41419-019-1612-3
PMC
PMC6522539
OpenAlex
W2946016906
Cited by
149
References
3
Citations by year
2026: 12 · 2025: 15 · 2024: 31 · 2023: 25 · 2022: 29 · 2021: 17 · 2020: 17 · 2019: 2
FWCI
12.87
Type
journal article
Language
en
Update notices
correction (2019-06-21)
Open access
Licence
Locations
  • Cell Death and Disease (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
Funders
  • National Natural Science Foundation of China (81571270, 31571168, 81770328)
  • 13th Talents Project of Jiangsu Province (JY-049) to Lei Chen
Topics
  • Health Sciences › Medicine › Clinical Neurology › Epilepsy research and treatment
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
Keywords
TRPV4, temporal lobe epilepsy, neuroinflammation, neuronal cell death, NLRP3 inflammasome, caspase-1, inflammatory cytokines, microglial activation, astrocyte activation, pilocarpine-induced status epilepticus, GSK1016790A, HC-067047, IL-1β, TNF-α, interleukin-6, neuroprotection, hippocampus, Ac-YVAD-cmk
MeSH terms
Animals, Astrocytes, Epilepsy, Temporal Lobe, Inflammation, Leucine, Male, Mice, Inbred ICR, Morpholines, Neurons, Pilocarpine, Pyrroles, Status Epilepticus, Sulfonamides, Microglia, TRPV Cation Channels, Mice, Inflammasomes

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