长链非编码 RNA TUG1 通过 miR-142-5p/SOCS1 轴调控溃疡性结肠炎。
lncRNA TUG1 regulates ulcerative colitis through miR-142-5p/SOCS1 axis.
机构信息
Department of Gastroenterology, The East Branch of the Second Hospital of Hebei Medical University, No.80 Huanghe Road, Shijiazhuang, 050000, Hebei, China; Department of Physical Examination Center, The North Branch of the Second Hospital of Hebei Medical University, No. 309 Zhonghua Street, Shijiazhuang, 050000, Hebei, China.
Department of Cardiology, The Third Hospital of Shijiazhuang, No. 15 Tiyu Street, Shijiazhuang, 050000, Hebei, China.
出版信息
Microb Pathog. 2020 Jun;143:104139. doi: 10.1016/j.micpath.2020.104139. Epub 2020 Mar 12.
Ulcerative colitis (UC) is a long-lasting inflammation disease which finally results in ulcer of the colon and rectum. The long non-coding RNA (lncRNA) TUG1 has been described to target miR-142 and regulate its expression. In current study, we evaluated the effects of long non-coding RNA TUG1 on cell injury and inflammatory cytokine production using a TNFα-treated HT-29 cells model. We monitored the level of TUG1 in colonic mucosa tissue of UC patients and in TNF-α-treated HT-29 cells. We investigated the effects of TUG1 on miR-142-5p and SOCS1expression, cell viability, lactate dehydrogenase (LDH) release, production of nitrite and PGE2 after TNF-α treatment in HT-29 cells. We also investigated the effects of TUG1 on TNF-α-induced IL-6, IL-8 and IL-1β expression in HT-29 cells. We detected down-regulated TUG1 level in colonic mucosa tissue of UC patients and in TNF-α-treated HT-29 cells. Overexpression of TUG1 enhanced cell viability, decreased LDH release, decreased nitrite and PGE2 production after TNF-α treatment in HT-29 cells. TUG1 prevented IL-1β, IL-6 and IL-8 production in TNF-α-treated cells. TUG1 targeted miR-142-5p and inhibited its expression while enhanced SOCS1 expression. Overexpression of miR-142-5p abolished TUG1-mediated inhibition of TNF-induced inflammatory cytokines production. TUG1 negatively regulated inflammation in ulcerative colitis through miR-142-5p/SOCS1 axis.
溃疡性结肠炎（UC）是一种长期存在的炎症性疾病，最终导致结肠和直肠溃疡。长链非编码 RNA（lncRNA）TUG1 已被描述为靶向 miR-142 并调节其表达。在目前的研究中，我们使用 TNFα 处理的 HT-29 细胞模型评估了长链非编码 RNA TUG1 对细胞损伤和炎症细胞因子产生的影响。我们监测了 UC 患者结肠黏膜组织和 TNF-α 处理的 HT-29 细胞中 TUG1 的水平。我们研究了 TUG1 对 miR-142-5p 和 SOCS1 表达、细胞活力、乳酸脱氢酶（LDH）释放、TNF-α 处理后 HT-29 细胞中亚硝酸盐和 PGE2 产生的影响。我们还研究了 TUG1 对 TNF-α 诱导的 HT-29 细胞中 IL-6、IL-8 和 IL-1β 表达的影响。我们检测到 UC 患者结肠黏膜组织和 TNF-α 处理的 HT-29 细胞中 TUG1 水平下调。在 TNF-α 处理的 HT-29 细胞中，过表达 TUG1 增强了细胞活力，降低了 LDH 释放，减少了 TNF-α 处理后亚硝酸盐和 PGE2 的产生。TUG1 抑制了 TNF-α 处理细胞中 IL-1β、IL-6 和 IL-8 的产生。TUG1 靶向 miR-142-5p 并抑制其表达，同时增强 SOCS1 表达。过表达 miR-142-5p 消除了 TUG1 介导的对 TNF 诱导的炎症细胞因子产生的抑制作用。TUG1 通过 miR-142-5p/SOCS1 轴负调控溃疡性结肠炎中的炎症。
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