Long Non-Coding RNA ANRIL Regulates Inflammatory Factor Expression in Ulcerative Colitis Via the miR-191-5p/SATB1 Axis

作者全名："Yu, Ke-Qi; Li, Chuan-Fei; Ye, Lu; Song, Ya; Wang, Yan-Hui; Lin, Yu-Ru; Liao, Sheng-Tao; Mei, Zhe-Chuan; Lv, Lin"

作者地址："[Yu, Ke-Qi; Li, Chuan-Fei; Ye, Lu; Song, Ya; Wang, Yan-Hui; Lin, Yu-Ru; Liao, Sheng-Tao; Mei, Zhe-Chuan; Lv, Lin] Chongqing Med Univ, Dept Gastroenterol, Affiliated Hosp 2, 74 Linjiang Rd, Chongqing 400010, Peoples R China"

通信作者："Liao, ST; Mei, ZC; Lv, L (通讯作者)，Chongqing Med Univ, Dept Gastroenterol, Affiliated Hosp 2, 74 Linjiang Rd, Chongqing 400010, Peoples R China."

来源：INFLAMMATION

ESI学科分类：IMMUNOLOGY

WOS号：WOS:001103608500001

JCR分区：Q2

影响因子：5.1

年份：2023

卷号：　

期号：　

开始页：　

结束页：　

文献类型：Article; Early Access

关键词：lncRNA ANRIL; miR-191-5p; SATB1; UC.

摘要："Ulcerative colitis, an inflammatory bowel disease, manifests with symptoms such as abdominal pain, diarrhea, and mucopurulent feces. The long non-coding RNA (lncRNA) ANRIL exhibits significantly reduced expression in UC, yet its specific mechanism is unknown. This study revealed that ANRIL is involved in the progression of UC by inhibiting IL-6 and TNF-alpha via miR-191-5P/SATB1 axis. We found that in patients with UC, interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) were significantly overexpressed in inflamed colon sites, whereas ANRIL was significantly under-expressed and associated with disease severity. The downregulation of ANRIL resulted in the increased expression of IL-6 and TNF-alpha in LPS-treated FHCs. ANRIL directly targeted miR-191-5p, thereby inhibiting its expression and augmenting SATB1 expression. Moreover, overexpression of miR-191-5p abolished ANRIL-mediated inhibition of IL-6 and TNF-alpha production. Dual luciferase reporter assays revealed the specific binding of miR-191-5p to ANRIL and SATB1. Furthermore, the downregulation of ANRIL promoted DSS-induced colitis in mice. Together, we provide evidence that ANRIL plays a critical role in regulating IL-6 and TNF-alpha expression in UC by modulating the miR-191-5p/SATB1 axis. Our study provides novel insights into progression and molecular therapeutic strategies in UC."

基金机构：Not applicable.

基金资助正文：Not applicable.