亲爱的研友该休息了!由于当前在线用户较少,发布求助请尽量完整的填写文献信息,科研通机器人24小时在线,伴您度过漫漫科研夜!身体可是革命的本钱,早点休息,好梦!

Decreased PDLIM1 expression in endothelial cells contributes to the development of intracranial aneurysm

医学 基因沉默 Wnt信号通路 细胞生物学 细胞周期蛋白D1 异位表达 信号转导 体内 癌症研究 分子生物学 生物 基因 细胞周期 遗传学
作者
Yan Yan,Xuanfeng Qin,Yongtao Zheng,Tao Jin,Yuanyuan Hu,Qingzhu An,Bing Leng
出处
期刊:Vascular Medicine [SAGE]
卷期号:29 (1): 5-16
标识
DOI:10.1177/1358863x231218210
摘要

Introduction: Intracranial aneurysm (IA) is a common vascular enlargement that occurs in the wall of cerebral vessels and frequently leads to fatal subarachnoid hemorrhage. PDZ and LIM domain protein 1 (PDLIM1) is a cytoskeletal protein that functions as a platform for multiple protein complex formation. However, whether PDLIM is involved in the pathogenesis of IA remains poorly understood. Methods: Loss-of-function and gain-of-function strategies were employed to determine the in vitro roles of PDLIM1 in vascular endothelial cells (VECs). A rat model of IA was generated to study the role of PDLIM1 in vivo. Gene expression profiling, Western blotting, and dual luciferase reporter assays were performed to uncover the underlying cellular mechanism. Clinical IA samples were used to determine the expression of PDLIM1 and its downstream signaling molecules. Results: PDLIM1 expression was reduced in the endothelial cells of IA and was regulated by Yes-associated protein 1 (YAP1). Genetic silencing of PDLIM1 inhibited the viability, migratory ability, and tube formation ability of VECs. Opposite results were obtained by ectopic expression of PDLIM1. Additionally, PDLIM1 overexpression mitigated IA in vivo. Mechanistic investigations revealed that PDLIM1 promoted the transcriptional activity of β-catenin and induced the expression of v-myc myelocytomatosis viral oncogene homolog (MYC) and cyclin D1 (CCND1). In clinical settings, reduced expression of PDLIM1 and β-catenin downstream target genes was observed in human IA samples. Conclusion: Our study indicates that YAP1-dependent expression of PDLIM1 can inhibit IA development by modulating the activity of the Wnt/β-catenin signaling pathway and that PDLIM1 deficiency in VECs may represent a potential marker of aggressive disease.
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
18秒前
zxq1996完成签到 ,获得积分10
20秒前
顾矜应助krajicek采纳,获得10
27秒前
30秒前
hzc应助科研通管家采纳,获得10
38秒前
44秒前
krajicek发布了新的文献求助10
49秒前
这个手刹不太灵完成签到 ,获得积分10
1分钟前
1分钟前
CUN完成签到,获得积分10
1分钟前
1分钟前
豪豪完成签到,获得积分10
2分钟前
2分钟前
hzc应助科研通管家采纳,获得10
2分钟前
hzc应助科研通管家采纳,获得10
2分钟前
2分钟前
3分钟前
大胆的凡儿完成签到 ,获得积分10
3分钟前
ding应助kukudou2采纳,获得10
3分钟前
souther完成签到,获得积分0
3分钟前
yfy完成签到 ,获得积分10
3分钟前
奔跑的蒲公英完成签到,获得积分10
4分钟前
不安初彤完成签到,获得积分10
4分钟前
4分钟前
CSun完成签到,获得积分10
4分钟前
4分钟前
kukudou2发布了新的文献求助10
4分钟前
CSun发布了新的文献求助10
4分钟前
桐桐应助不安初彤采纳,获得10
4分钟前
kukudou2完成签到,获得积分10
4分钟前
hzc应助科研通管家采纳,获得10
4分钟前
yyy发布了新的文献求助10
5分钟前
5分钟前
6分钟前
6分钟前
6分钟前
hzc应助科研通管家采纳,获得10
6分钟前
7分钟前
不安初彤发布了新的文献求助10
7分钟前
7分钟前
高分求助中
The ACS Guide to Scholarly Communication 2500
Sustainability in Tides Chemistry 2000
Studien zur Ideengeschichte der Gesetzgebung 1000
TM 5-855-1(Fundamentals of protective design for conventional weapons) 1000
Threaded Harmony: A Sustainable Approach to Fashion 810
Pharmacogenomics: Applications to Patient Care, Third Edition 800
Free Will in the Flesh 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 3081574
求助须知:如何正确求助?哪些是违规求助? 2734422
关于积分的说明 7532754
捐赠科研通 2383882
什么是DOI,文献DOI怎么找? 1264077
科研通“疑难数据库(出版商)”最低求助积分说明 612563
版权声明 597578