Suppr超能文献

miR-186,一种血清 microRNA,通过靶向 SMAD6 在川崎病中诱导内皮细胞凋亡。

miR‑186, a serum microRNA, induces endothelial cell apoptosis by targeting SMAD6 in Kawasaki disease.

机构信息

Children's Heart Center, Institute of Cardiovascular Development and Translational Medicine, The Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325027, P.R. China.

Wenzhou Medical University, Wenzhou, Zhejiang 325035, P.R. China.

出版信息

Int J Mol Med. 2018 Apr;41(4):1899-1908. doi: 10.3892/ijmm.2018.3397. Epub 2018 Jan 18.

Abstract

Kawasaki disease (KD) is an acute, self‑limited vasculitis that predominantly affects medium‑sized arteries, particularly the coronary arteries. Recent studies have indicated that microRNAs are involved in many diseases, including KD. However, the detailed mechanism remains unclear. The aim of the present study was to explore the role of miR‑186 in KD and potentially discover a new target for KD treatment. The results demonstrated that miR‑186 was upregulated in serum from patients with KD and KD serum could increase miR‑186 transcript levels in endothelial cells (HUVECs). Overexpression of miR‑186 mimic induced HUVEC apoptosis through mitogen‑activated protein kinase (MAPK) activation by targeting and inhibiting SMAD family member 6 (SMAD6). Furthermore, KD serum induced HUVEC apoptosis through miR‑186. In conclusion, the present results suggested that KD serum‑associated miR‑186 has an essential role in endothelial cell apoptosis by activating the MAPK pathway through targeting the SMAD6 gene.

摘要

川崎病(KD)是一种主要影响中型动脉,特别是冠状动脉的急性、自限性血管炎。最近的研究表明,microRNAs 参与了许多疾病,包括 KD。然而,其详细机制尚不清楚。本研究旨在探讨 miR-186 在 KD 中的作用,并可能为 KD 治疗发现新的靶点。结果表明,KD 患者血清中的 miR-186 上调,KD 血清可增加内皮细胞(HUVEC)中的 miR-186 转录水平。miR-186 模拟物的过表达通过靶向和抑制 SMAD 家族成员 6(SMAD6)来激活丝裂原活化蛋白激酶(MAPK),诱导 HUVEC 凋亡。此外,KD 血清通过 miR-186 诱导 HUVEC 凋亡。综上所述,本研究结果表明,KD 相关血清 miR-186 通过靶向 SMAD6 基因激活 MAPK 通路,在血管内皮细胞凋亡中发挥重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a2d/5810213/aa9e967beb31/IJMM-41-04-1899-g00.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验