Microglial PCGF1 alleviates neuroinflammation associated depressive behavior in adolescent mice

神经炎症 小胶质细胞 神经科学 心理学 抑郁症状 医学 炎症 认知 免疫学
作者
Naigang Li,Jingyi Du,Ying Yang,Tiantian Zhao,Dong Wu,Fan Peng,Dongshuang Wang,Linghua Kong,Wenjuan Zhou,Aijun Hao
出处
期刊:Molecular Psychiatry [Springer Nature]
卷期号:30 (3): 914-926 被引量:19
标识
DOI:10.1038/s41380-024-02714-2
摘要

Epigenetics plays a crucial role in regulating gene expression during adolescent brain maturation. In adolescents with depression, microglia-mediated chronic neuroinflammation may contribute to the activation of cellular signaling cascades and cause central synapse loss. However, the exact mechanisms underlying the epigenetic regulation of neuroinflammation leading to adolescent depression remain unclear. In this study, we found that the expression of polycomb group 1 (PCGF1), an important epigenetic regulator, was decreased both in the plasma of adolescent major depressive disorder (MDD) patients and in the microglia of adolescent mice in a mouse model of depression. We demonstrated that PCGF1 alleviates neuroinflammation mediated by microglia in vivo and in vitro, reducing neuronal damage and improving depression-like behavior in adolescent mice. Mechanistically, PCGF1 inhibits the transcription of MMP10 by upregulating RING1B/H2AK119ub and EZH2/H3K27me3 in the MMP10 promoter region, specifically inhibiting microglia-mediated neuroinflammation. These results provide valuable insights into the pathogenesis of adolescent depression, highlighting potential links between histone modifications, neuroinflammation and nerve damage. Potential mechanisms of microglial PCGF1 regulates depression-like behavior in adolescent mice. Microglial PCGF1 inhibits NF-κB/MAPK pathway activation through regulation of RING1B/H2AK119ub and EZH2/H3K27me3 in the MMP10 promoter region, which attenuates neuroinflammation and ameliorates depression-like behaviors in adolescent mice.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
刚刚
Elias完成签到 ,获得积分10
1秒前
蓝天发布了新的文献求助10
1秒前
晴朗同学完成签到,获得积分10
2秒前
曾经的尔曼完成签到,获得积分10
2秒前
2秒前
Akim应助怕孤独的白容采纳,获得10
3秒前
威武的血茗完成签到,获得积分10
3秒前
6秒前
源源完成签到,获得积分10
6秒前
圈圈黄发布了新的文献求助20
6秒前
高高完成签到,获得积分10
6秒前
7秒前
fragile完成签到,获得积分10
8秒前
眯眯眼的代容完成签到,获得积分10
8秒前
晨露完成签到 ,获得积分10
9秒前
好奇的书蛋完成签到,获得积分10
10秒前
脑洞疼应助小雪采纳,获得10
11秒前
Hello应助RttTde采纳,获得10
12秒前
干净老姆完成签到,获得积分10
12秒前
13秒前
Skilixta完成签到,获得积分10
15秒前
科研通AI6.4应助大气归尘采纳,获得10
15秒前
高大以南完成签到,获得积分10
17秒前
jjding完成签到,获得积分10
17秒前
18秒前
欢喜雯发布了新的文献求助10
18秒前
19秒前
20秒前
molihuakai应助xinze采纳,获得10
21秒前
liang完成签到 ,获得积分10
22秒前
22秒前
Copyright应助DG采纳,获得10
22秒前
小铭同学完成签到,获得积分10
22秒前
22秒前
嘻嘻完成签到,获得积分10
22秒前
欣慰的雨旋完成签到 ,获得积分10
23秒前
小柒完成签到 ,获得积分10
23秒前
Frank完成签到 ,获得积分10
23秒前
xhjh03发布了新的文献求助10
23秒前
高分求助中
Principles of Economics, 11th Edition 10000
University Physics with Modern Physics, 16th edition 10000
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Gründe der Seele:Die Wiener Psychatrie im 20.Jahrhundert 1000
Development of a Bridge Weigh-In-Motion System: A technology to convert the bridge response to the passage of traffic into data on vehicle configurations, speeds, times of travel and weights 1000
Organic Reactions, Volume 116 1000
Current concepts in cutaneous toxicity : proceedings of the Fourth Conference on Cutaneous Toxicity, Washington, D.C., May 9-11, 1979 1000
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 工程类 有机化学 化学工程 生物化学 计算机科学 内科学 物理 复合材料 催化作用 细胞生物学 无机化学 光电子学 物理化学 电极 基因
热门帖子
关注 科研通微信公众号,转发送积分 7270827
求助须知:如何正确求助?哪些是违规求助? 8891121
关于积分的说明 18795070
捐赠科研通 6945729
什么是DOI,文献DOI怎么找? 3203794
关于科研通互助平台的介绍 2376656
邀请新用户注册赠送积分活动 2179734