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[1]張潤民,鄭崢,劉德山.CD2關(guān)聯(lián)蛋白通過PI3K/Akt信號通路調(diào)節(jié)神經(jīng)瘤細胞N2A的神經(jīng)突觸生長[J].福建醫(yī)藥雜志,2025,47(04):77-80.[doi:10.20148/j.fmj.2025.04.021]
　ZHANG Runmin,ZHENG Zheng,LIU Deshan.CD2-associated protein regulates neurite outgrowth in Neuro2a(N2A)cells via the PI3K/Akt signaling pathway[J].FUJIAN MEDICAL JOURNAL,2025,47(04):77-80.[doi:10.20148/j.fmj.2025.04.021]
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CD2關(guān)聯(lián)蛋白通過PI3K/Akt信號通路調(diào)節(jié)神經(jīng)瘤細胞N2A的神經(jīng)突觸生長()
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《福建醫(yī)藥雜志》[ISSN:1002-2600/CN:35-1071/R]

卷:
47
期數(shù):
2025年04期
頁碼:
77-80
欄目:
基礎(chǔ)研究
出版日期:
2025-04-20

文章信息/Info

Title:
CD2-associated protein regulates neurite outgrowth in Neuro2a(N2A)cells via the PI3K/Akt signaling pathway
文章編號:
1002-2600(2025)04-0077-04
作者:
張潤民; 鄭崢; 劉德山
福州大學附屬省立醫(yī)院,福州 350001
Author(s):
ZHANG Runmin;  ZHENG Zheng;  LIU Deshan
Department of Neurology, Fuzhou University Affiliated Provincial Hospital, Fuzhou, Fujian 350001, China
關(guān)鍵詞:
阿爾茨海默病;  CD2關(guān)聯(lián)蛋白;  突觸可塑性;  認知損害
Keywords:
Alzheimer's disease;  CD2-associated protein;  synaptic plasticity;  cognitive impairment
分類號:
R736.1,R445
DOI:
10.20148/j.fmj.2025.04.021
文獻標志碼:
B
摘要:
目的 探討CD2關(guān)聯(lián)蛋白(CD2-associated protein,CD2AP)調(diào)節(jié)神經(jīng)瘤細胞N2A(Neuro2a,N2A)的神經(jīng)突觸生長可能的作用機制。方法 應用shRNA CD2AP和過表達CD2AP的慢病毒感染N2A細胞,有效下調(diào)和上調(diào)CD2AP后,通過免疫共沉淀(Co-Immunoprecipitation,Co-IP)等方法研究CD2AP、PI3K和TrkA等蛋白的相互作用關(guān)系,探討CD2AP是否通過PI3K/Akt信號通路調(diào)節(jié) N2A細胞的神經(jīng)突觸的生長。結(jié)果 在全反式維甲酸(all-trans retinoic acid, ATRA)刺激N2A細胞后,CD2AP支架蛋白可以與TrkA受體發(fā)生相互作用,繼續(xù)激活PI3K/Akt信號通路相關(guān)蛋白的表達。在ATRA干預N2A細胞中,TrkA與CD2AP之間存在共定位,并形成TrkA-CD2AP復合物,進一步證實CD2AP是在神經(jīng)突起結(jié)構(gòu)可塑性中Akt通路的一個正調(diào)控的因子。結(jié)論 CD2AP通過PI3K/Akt信號通路調(diào)節(jié)N2A細胞的神經(jīng)突觸生長。
Abstract:
Objective To explore the possible mechanism of neuronal growth of CD2-associated protein(CD2AP)to regulate Neuro2a cells. Methods N2A cells were infected with shRNACD2AP and lentivirus overexpressed CD2AP to effectively down-regulate and up-regulate CD2AP. The interaction among CD2AP, PI3K and TrkA proteins was investigated by methods such as Co-immunoprecipitation(Co-IP), and the role of CD2AP in regulating the growth of neurites in N2A cells through the PI3K/Akt signaling pathway was explored. Results After all-trans retinoic acid(ATRA)stimulation of N2A cells, the CD2AP scaffold protein can interact with the TrkA receptor, further activating the expression of proteins related to the PI3K/Akt signaling pathway. In ATRA-intervened N2A cells, TrkA and CD2AP co-localize and form a TrkA-CD2AP complex, further confirming that CD2AP is a positive regulatory factor of the Akt pathway in the structural plasticity of neurites.Conclusion CD2AP regulates the synaptic growth of Neuro2a cells through PI3K/Akt signaling pathway.

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備注/Memo

備注/Memo:
基金項目:福建省自然科學基金項目(2023J011201)
通信作者:劉德山,Email: [email protected]
更新日期/Last Update: 2025-04-20