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
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.
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