GRIN2B alleviates mid-gestational sevoflurane exposure-induced early differentiation of rat neural stem cells by interacting with KIF17

IF 3.6 3区 生物学 Q3 CELL BIOLOGY
Mengyuan Li, Yan Hu, Zhonggui Cheng, Qianqian Li
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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.

Abstract Image

GRIN2B通过与KIF17相互作用减轻妊娠中期七氟醚暴露诱导的大鼠神经干细胞的早期分化
怀孕期间的全身麻醉暴露对发育中的大脑有神经毒性作用,导致后代长期的认知功能障碍。妊娠中期暴露于七氟醚导致神经干细胞(NSCs)过早分化,是影响正常海马功能和导致神经认知障碍的关键因素。然而,相关的分子机制尚不清楚。在体内试验中,妊娠大鼠在妊娠第14天(G14)暴露于3%七氟醚1次,或在妊娠第13、14和15天暴露于3%七氟醚3次(每天2小时)。对于体外实验,在出生后24和72小时以及出生后28天从胎儿海马组织中分离出原代大鼠NSCs。在连续暴露于4.1%七氟醚1天或3天(每天2小时)之前,转染了GRIN2B或KIF17过表达质粒的NSCs。孕中期多次暴露于七氟醚可导致子代大鼠和原代大鼠NSCs海马中GRIN2B和KIF17的表达降低,NSC过早分化。GRIN2B或KIF17过表达可减弱七氟醚诱导的NSC过早分化。GRIN2B与KIF17相互作用,KIF17沉默逆转了GRIN2B过表达对NSC早期分化的抑制作用。GRIN2B通过与KIF17的相互作用减轻妊娠中期反复暴露于七氟醚诱导的NSC过早分化。
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来源期刊
CiteScore
6.40
自引率
4.90%
发文量
40
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.
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