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Suppression of TRPV5 Regulates Microglia-Mediated Neuroinflammation Following Status Epilepticus

Authors
 Park, Soojin  ;  Kim, Se Hoon  ;  Kim, Chul Hoon  ;  Jeong, Kyoung Hoon  ;  Kim, Won-Joo 
Citation
 GLIA, , 2025-07 
Journal Title
GLIA
ISSN
 0894-1491 
Issue Date
2025-07
MeSH
Animals ; Cells, Cultured ; Hippocampus / drug effects ; Hippocampus / metabolism ; Hippocampus / pathology ; Male ; Mice ; Mice, Inbred C57BL ; Microglia* / drug effects ; Microglia* / metabolism ; Neuroinflammatory Diseases* / metabolism ; Neuroinflammatory Diseases* / pathology ; Pilocarpine / toxicity ; Status Epilepticus* / chemically induced ; Status Epilepticus* / metabolism ; Status Epilepticus* / pathology ; TRPV Cation Channels* / antagonists & inhibitors ; TRPV Cation Channels* / metabolism
Keywords
econazole ; microglia ; neuroinflammation ; status epilepticus ; TRPV5
Abstract
Neuroinflammation, predominantly associated with glial activation and the release of various inflammatory mediators, is a vital hallmark of the pathophysiology of epilepsy. Numerous studies have indicated that identifying novel factors that diminish neuroinflammatory processes may be important for developing effective therapeutic strategies to prevent neuropathological processes and epileptogenic progression. Transient receptor potential vanilloid 5 (TRPV5) is a highly selective calcium ion channel belonging to the TRPV family. TRPV5 expression has been identified in diverse regions of the brain; however, it remains unknown how TRPV5 is implicated in the pathophysiological features of neurological diseases, including epilepsy. Herein, we show that TRPV5 expression is upregulated in the hippocampus of a pilocarpine-induced status epilepticus (PCSE) model, predominantly in activated microglia. Pharmacological inhibition of TRPV5 using econazole attenuated microglial activation, as indicated by the shift of LPS-stimulated primary hippocampal microglia to a resting state. This inhibition suppressed AKT/NF-kappa B signaling, reduced NLRP3 inflammasome activity, and decreased proinflammatory cytokine production. Additionally, TRPV5 inhibition reduced hippocampal microglial activation and neuroinflammation following PCSE. These findings suggest that TRPV5 contributes to the regulation of microglial activation, resulting in the suppression of microglia-derived neuroinflammation during the sub-acute phase of epilepsy. In conclusion, the present study suggests that targeting TRPV5 may offer a novel therapeutic approach to managing the neuroinflammatory processes during epileptogenic progression.
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DOI
10.1002/glia.70068
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pathology (병리학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Pharmacology (약리학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Research Institute (부설연구소) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Neurology (신경과학교실) > 1. Journal Papers
Yonsei Authors
Kim, Se Hoon(김세훈) ORCID logo https://orcid.org/0000-0001-7516-7372
Kim, Won Joo(김원주) ORCID logo https://orcid.org/0000-0002-5850-010X
Kim, Chul Hoon(김철훈) ORCID logo https://orcid.org/0000-0002-7360-429X
Jeong, Kyoung Hoon(정경훈) ORCID logo https://orcid.org/0000-0002-6100-9936
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/207381
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