microRNA-650 promotes inflammation induced apoptosis of intestinal epithelioid cells by targeting NLRP6

溃疡性结肠炎 小RNA 炎症性肠病 结肠炎 细胞凋亡 发病机制 非翻译区 炎症 癌症研究 三素数非翻译区 生物 荧光素酶 下调和上调 基因 免疫学 转染 医学 信使核糖核酸 疾病 病理 遗传学
作者
Xiaoxia Xu,Xi Zhu,Chenyang Wang,Yang Li,Caibin Fan,Xiaoming Kao
出处
期刊:Biochemical and Biophysical Research Communications [Elsevier BV]
卷期号:517 (4): 551-556 被引量:16
标识
DOI:10.1016/j.bbrc.2019.06.077
摘要

Ulcerative colitis (UC), a serious threat to public health, is one of the main forms of inflammatory bowel disease, whereas the molecular mechanisms underlying ulcerative colitis induced by inflammation still remain elusive. NPLR6 gene is previously shown to regulate intestinal homeostasis and regulate the colonic microbial ecology. Here, we report that microRNA-650 (miR-650) plays an important role in the pathogenesis of UC as an upstream regulator of NPLR6 gene. MiR-650 is proved overexpressed in the inflamed mucosa of patients with ulcerative colitis and the DSS induced colitis model mice by qRT-PCR. Over-expression of miR-650 leads to increased apoptosis of Caco-2 and IEC-6 cells, and the DSS-induced mice aggravation, while knock-down of miR-650 shows opposite effects. Through constructing luciferase reporter genes containing 3'-untranslated regions of NLRP6, we further demonstrate that miR-650 inhibits NLRP6 through binding to its 3'-untranslated regions. Overexpression of NLRP6 in Caco-2 and IEC-6 cells suppress the increase apoptosis induced by miR-650 overexpression. Overall, the findings of this study indicate the role of miR-650 in ulcerative colitis, which provides a new target for therapeutic treatment.

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
CNYDNZB完成签到,获得积分10
刚刚
xuelanghu发布了新的文献求助10
2秒前
3秒前
3秒前
4秒前
arniu2008应助橙留香采纳,获得20
4秒前
打打应助橘柚采纳,获得30
5秒前
5秒前
zl完成签到,获得积分10
5秒前
kk完成签到,获得积分20
6秒前
早起发布了新的文献求助10
6秒前
科研小菜鸡完成签到,获得积分10
7秒前
7秒前
7秒前
lch发布了新的文献求助10
8秒前
8秒前
cc发布了新的文献求助10
8秒前
9秒前
9秒前
10秒前
lucas完成签到,获得积分10
10秒前
11秒前
11秒前
11秒前
12秒前
呼呼呼发布了新的文献求助10
12秒前
小蘑菇应助dreamland黎锦采纳,获得30
13秒前
13秒前
传奇3应助马铭泽采纳,获得10
13秒前
13秒前
科研通AI2S应助欣潔采纳,获得10
15秒前
drfwjuikesv发布了新的文献求助10
16秒前
Orange应助科大第一深情采纳,获得10
16秒前
一一发布了新的文献求助10
16秒前
16秒前
陈贞月发布了新的文献求助10
17秒前
congcong完成签到,获得积分10
17秒前
17秒前
17秒前
18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
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
Molecular Mechanisms of Photosynthesis, 4th Edition 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 7262171
求助须知:如何正确求助?哪些是违规求助? 8883538
关于积分的说明 18774069
捐赠科研通 6941399
什么是DOI,文献DOI怎么找? 3202412
关于科研通互助平台的介绍 2375640
邀请新用户注册赠送积分活动 2178094