Dysregulation of immune and metabolism pathways in maternal immune activation induces an increased risk of autism spectrum disorders

后代 免疫系统 生物 表观遗传学 自闭症 自闭症谱系障碍 胚胎干细胞 免疫失调 基因 生物信息学 遗传学 怀孕 医学 精神科
作者
Huamin Yin,Zhendong Wang,Jiaxin Liu,Ying Li,Li Liu,Peijun Huang,Wenhang Wang,Zhiyan Shan,Ruizhen Sun,Jingling Shen,Lian Duan
出处
期刊:Life Sciences [Elsevier]
卷期号:324: 121734-121734 被引量:10
标识
DOI:10.1016/j.lfs.2023.121734
摘要

Maternal immune activation (MIA) via infection during pregnancy is known to be an environmental risk factor for neurodevelopmental disorders and the development of autism spectrum disorders (ASD) in the offspring, but it still remains elusive that the molecular relevance between infection-induced abnormal neurodevelopmental events and an increased risk for ASD development. Fully considering the extremely high genetic heterogeneity of ASD and the universality of risk-gene with minimal effect-sizes, the gene and pathway-based association analysis was performed with the transcriptomic and DNA methylation landscapes of temporal human embryonic brain development and ASD, and the time-course transcriptional profiling of MIA. We conducted the transcriptional profiling of mouse abnormal neurodevelopment two days following induced MIA via LPS injection at E10.5. A novel evidence was proved that illustrated altering four immune and metabolism-related risk pathways, including starch and sucrose metabolism, ribosome, protein processing in endoplasmic reticulum, and retrograde endocannabinoid signaling pathway, which were prominent involvement in the process of MIA regulating abnormal fetal brain development to induce an increased risk of ASD. Here, we have observed that almost all key genes within these risk pathways are significantly differentially expressed at embryonic days (E) 10.5–12.5, which is considered to be the optimal coincidence window of mouse embryonic brain development to study the intimate association between MIA and ASD using mouse animal models. There search establishes that MIA causes dysregulation of immune and metabolic pathways, which leads to abnormal embryonic neurodevelopment, thus promoting development of ASD symptoms in offspring.
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
更新
大幅提高文件上传限制,最高150M (2024-4-1)

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
抱小熊睡觉完成签到,获得积分10
刚刚
明理寄云发布了新的文献求助10
刚刚
刚刚
强健的电话完成签到,获得积分20
刚刚
SWD完成签到,获得积分10
1秒前
西瓜西瓜完成签到,获得积分10
1秒前
1秒前
lbw完成签到,获得积分10
1秒前
2秒前
2秒前
颖中竹子完成签到,获得积分10
3秒前
冷傲板栗发布了新的文献求助10
3秒前
3秒前
3秒前
4秒前
拼搏的忆寒完成签到,获得积分20
4秒前
劲秉应助昂口3采纳,获得10
5秒前
华仔应助bbamx采纳,获得10
5秒前
Chris发布了新的文献求助10
5秒前
无花果应助欣欣然采纳,获得10
5秒前
CLN完成签到,获得积分10
5秒前
宁宁发布了新的文献求助10
7秒前
星星完成签到,获得积分10
7秒前
科研通AI2S应助耍酷的白山采纳,获得10
7秒前
酷波er应助Wiesen采纳,获得10
7秒前
高尚发布了新的文献求助10
8秒前
8秒前
东方诩发布了新的文献求助10
8秒前
xhuryts完成签到,获得积分10
9秒前
laxy完成签到,获得积分10
9秒前
狂野萤应助雾野与晚风采纳,获得20
9秒前
慕课魔芋发布了新的文献求助10
11秒前
神行太保完成签到,获得积分10
12秒前
0128lun应助ElbingX采纳,获得20
12秒前
冷傲板栗完成签到,获得积分10
13秒前
忆韵发布了新的文献求助10
13秒前
13秒前
Zhihu完成签到,获得积分10
13秒前
15秒前
Orange应助Leo采纳,获得10
15秒前
高分求助中
Evolution 3rd edition 1500
保险藏宝图 1000
Lire en communiste 1000
Mantiden: Faszinierende Lauerjäger Faszinierende Lauerjäger 700
PraxisRatgeber: Mantiden: Faszinierende Lauerjäger 700
A new species of Coccus (Homoptera: Coccoidea) from Malawi 500
2-Acetyl-1-pyrroline: an important aroma component of cooked rice 500
热门求助领域 (近24小时)
化学 医学 生物 材料科学 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 基因 遗传学 催化作用 物理化学 免疫学 量子力学 细胞生物学
热门帖子
关注 科研通微信公众号,转发送积分 3184082
求助须知:如何正确求助?哪些是违规求助? 2834357
关于积分的说明 7999302
捐赠科研通 2496567
什么是DOI,文献DOI怎么找? 1332442
科研通“疑难数据库(出版商)”最低求助积分说明 636579
邀请新用户注册赠送积分活动 603868