{"title":"GRIN2B alleviates mid-gestational sevoflurane exposure-induced early differentiation of rat neural stem cells by interacting with KIF17","authors":"Mengyuan Li, Yan Hu, Zhonggui Cheng, Qianqian Li","doi":"10.1002/ccs3.70024","DOIUrl":null,"url":null,"abstract":"<p>General anesthetic exposure during pregnancy has neurotoxic effects on the developing brain, causing long-term cognitive dysfunction in the offspring. Sevoflurane exposure during mid-gestation results in premature differentiation of neural stem cells (NSCs), being the crucial factor affecting normal hippocampal functions and contributing to neurocognitive impairment. However, the related molecular mechanism remains unclear. For in vivo assays, pregnant rats were exposed to 3% sevoflurane once on gestational day 14 (G14) or 3 times on G13, 14, and 15 (2 h per day). For in vitro assays, primary rat NSCs were isolated from fetal hippocampus tissues at 24 and 72 h after birth and on postnatal day 28. NSCs were transfected with GRIN2B or KIF17 overexpression plasmids before exposure to 4.1% sevoflurane for one or three consecutive days (2 h per day). Multiple sevoflurane exposures during the mid-trimester triggered NSC premature differentiation and decreased GRIN2B and KIF17 expression in the hippocampus of offspring rats and primary rat NSCs. GRIN2B or KIF17 overexpression attenuated sevoflurane-induced NSC premature differentiation. GRIN2B interacted with KIF17, and KIF17 silencing reversed the inhibition of GRIN2B overexpression on NSC early differentiation. GRIN2B alleviates NSC premature differentiation induced by repeated mid-gestational sevoflurane exposure via interaction with KIF17.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 2","pages":""},"PeriodicalIF":3.6000,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70024","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Cell Communication and Signaling","FirstCategoryId":"99","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/ccs3.70024","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
General anesthetic exposure during pregnancy has neurotoxic effects on the developing brain, causing long-term cognitive dysfunction in the offspring. Sevoflurane exposure during mid-gestation results in premature differentiation of neural stem cells (NSCs), being the crucial factor affecting normal hippocampal functions and contributing to neurocognitive impairment. However, the related molecular mechanism remains unclear. For in vivo assays, pregnant rats were exposed to 3% sevoflurane once on gestational day 14 (G14) or 3 times on G13, 14, and 15 (2 h per day). For in vitro assays, primary rat NSCs were isolated from fetal hippocampus tissues at 24 and 72 h after birth and on postnatal day 28. NSCs were transfected with GRIN2B or KIF17 overexpression plasmids before exposure to 4.1% sevoflurane for one or three consecutive days (2 h per day). Multiple sevoflurane exposures during the mid-trimester triggered NSC premature differentiation and decreased GRIN2B and KIF17 expression in the hippocampus of offspring rats and primary rat NSCs. GRIN2B or KIF17 overexpression attenuated sevoflurane-induced NSC premature differentiation. GRIN2B interacted with KIF17, and KIF17 silencing reversed the inhibition of GRIN2B overexpression on NSC early differentiation. GRIN2B alleviates NSC premature differentiation induced by repeated mid-gestational sevoflurane exposure via interaction with KIF17.
期刊介绍:
The Journal of Cell Communication and Signaling provides a forum for fundamental and translational research. In particular, it publishes papers discussing intercellular and intracellular signaling pathways that are particularly important to understand how cells interact with each other and with the surrounding environment, and how cellular behavior contributes to pathological states. JCCS encourages the submission of research manuscripts, timely reviews and short commentaries discussing recent publications, key developments and controversies.
Research manuscripts can be published under two different sections :
In the Pathology and Translational Research Section (Section Editor Andrew Leask) , manuscripts report original research dealing with celllular aspects of normal and pathological signaling and communication, with a particular interest in translational research.
In the Molecular Signaling Section (Section Editor Satoshi Kubota) manuscripts report original signaling research performed at molecular levels with a particular interest in the functions of intracellular and membrane components involved in cell signaling.