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
wangying完成签到,获得积分10
1秒前
1秒前
123456789完成签到,获得积分20
1秒前
感谢啾啾转发科研通微信,获得积分50
2秒前
优美丹雪发布了新的文献求助10
2秒前
彭于晏应助苍禾采纳,获得10
2秒前
3秒前
mm完成签到,获得积分10
3秒前
洋洋发布了新的文献求助20
4秒前
4秒前
MT完成签到 ,获得积分10
4秒前
4秒前
5秒前
感谢正直的语山转发科研通微信,获得积分50
5秒前
aizhujun发布了新的文献求助10
6秒前
6秒前
sunshine完成签到,获得积分10
7秒前
科目三应助柚子采纳,获得10
7秒前
7秒前
会撒娇的安南完成签到,获得积分10
7秒前
英姑应助HealthyCH采纳,获得10
8秒前
HHHHD发布了新的文献求助10
8秒前
8秒前
KD发布了新的文献求助10
8秒前
8秒前
chase完成签到,获得积分20
9秒前
9秒前
vn完成签到,获得积分10
9秒前
JLAlpaca发布了新的文献求助10
9秒前
无敌吴硕发布了新的文献求助10
10秒前
七分冷酷发布了新的文献求助10
10秒前
Twilight完成签到,获得积分10
10秒前
方法和歌完成签到,获得积分10
10秒前
叶子完成签到,获得积分20
11秒前
感谢797转发科研通微信,获得积分50
11秒前
Jasper应助优美丹雪采纳,获得10
12秒前
柯飞扬完成签到,获得积分10
12秒前
12秒前
Hello应助aizhujun采纳,获得10
12秒前
九九发布了新的文献求助10
12秒前
高分求助中
Spray / Wall-interaction Modelling by Dimensionless Data Analysis 2000
ALA生合成不全マウスでの糖代謝異常の分子機構解析 520
Aspects of Babylonian celestial divination: the lunar eclipse tablets of Enūma Anu Enlil 500
Mathematics and Finite Element Discretizations of Incompressible Navier—Stokes Flows 500
2024 Medicinal Chemistry Reviews 400
Dictionary of socialism 350
Mixed-anion Compounds 300
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 3198246
求助须知:如何正确求助?哪些是违规求助? 2847229
关于积分的说明 8062837
捐赠科研通 2512120
什么是DOI,文献DOI怎么找? 1343954
科研通“疑难数据库(出版商)”最低求助积分说明 639678
邀请新用户注册赠送积分活动 609316