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长链非编码 RNA SNHG5 通过 microRNA-375/Janus 激酶-2 轴调控溃疡性结肠炎。

Long non-coding RNA SNHG5 regulates ulcerative colitis via microRNA-375 / Janus kinase-2 axis.

机构信息

Department of Gastroenterology, Affiliated Hospital of Integrated Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China.

Department of Gastroenterology, Jinling Hospital, Nanjing, China.

出版信息

Bioengineered. 2021 Dec;12(1):4150-4158. doi: 10.1080/21655979.2021.1953219.

DOI:10.1080/21655979.2021.1953219
PMID:34334085
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8806617/
Abstract

Ulcerative colitis (UC) is an intestinal inflammatory disorder. Long non-coding RNAs (lncRNAs) are collectively involved in UC. This study is designed to explore the roles of lncRNA (small nucleolar RNA host gene 5) SNHG5 in UC. Gene or microRNA (miRNA) expression was detected using RT-qPCR and western blot, respectively. Cellular functions were analyzed by cell counting kit 8 (CCK8), 5-ethynyl-2'-deoxyuridine (EdU) assay, flow cytometry, and the terminal deoxyribonucleotidyl transferase (TDT)-mediated dUTP-digoxigenin nick end labeling (TUNEL) assays. Lactate dehydrogenase (LDH) content was determined by a cell cytotoxicity assay. The interactions between miR-375 and SNHG5 or Janus kinase-2 () were verified by a luciferase reporter assay. SNHG5 was up-regulated in intestinal mucosa tissues of UC patients as well as tumor necrosis factor alpha-treated (TNF-α-treated) young adult mouse colon (YAMC) cells. Down-regulated SNHG5 promoted cell proliferation and inhibited apoptosis of YAMC cells. miR-375 was verified to be a target of SNHG5 and was suppressed by TNF-α treatment in YAMC cells. Over-expression of miR-375 restored YAMC cellular functions. Additionally, miR-375 targeted , which was up-regulated by TNF-α treated YAMC cells. Up-regulation of induced the dysfunction of YAMC cells. Knockdown of SNHG5 promoted the proliferation and suppressed the apoptosis of YAMC cells via regulating miR-375/ axis. Therefore, knockdown of SNHG5 may be a promising therapy for UC.

摘要

溃疡性结肠炎（UC）是一种肠道炎症性疾病。长链非编码 RNA（lncRNA）共同参与 UC 的发生。本研究旨在探讨 lncRNA（核仁小 RNA 宿主基因 5）SNHG5 在 UC 中的作用。分别采用 RT-qPCR 和 Western blot 检测基因或 microRNA（miRNA）的表达。通过细胞计数试剂盒 8（CCK8）、5-乙炔基-2'-脱氧尿苷（EdU）测定、流式细胞术和末端脱氧核糖核苷酸转移酶（TDT）介导的脱氧尿苷三磷酸（dUTP）-地高辛尼克末端标记（TUNEL）测定分析细胞功能。通过细胞毒性测定确定乳酸脱氢酶（LDH）含量。通过荧光素酶报告基因测定验证 miR-375 与 SNHG5 或 Janus 激酶-2（）之间的相互作用。SNHG5 在 UC 患者的肠道黏膜组织以及肿瘤坏死因子-α处理（TNF-α 处理）的年轻成年鼠结肠（YAMC）细胞中上调。下调 SNHG5 促进 YAMC 细胞的增殖并抑制其凋亡。miR-375 被证实是 SNHG5 的靶标，并在 YAMC 细胞中被 TNF-α 处理所抑制。miR-375 的过表达恢复了 YAMC 细胞的功能。此外，miR-375 靶向 ，其在 TNF-α 处理的 YAMC 细胞中上调。上调的 诱导 YAMC 细胞功能障碍。SNHG5 的下调通过调节 miR-375/ 轴促进 YAMC 细胞的增殖并抑制其凋亡。因此，下调 SNHG5 可能是 UC 的一种有前途的治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7807/8806617/8ea6993f0d66/KBIE_A_1953219_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7807/8806617/5a7abc912673/KBIE_A_1953219_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7807/8806617/91b13b3f11d2/KBIE_A_1953219_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7807/8806617/7a8ec70b7129/KBIE_A_1953219_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7807/8806617/a9f789d0b933/KBIE_A_1953219_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7807/8806617/e1555fb706a4/KBIE_A_1953219_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7807/8806617/189b0496713f/KBIE_A_1953219_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7807/8806617/8ea6993f0d66/KBIE_A_1953219_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7807/8806617/5a7abc912673/KBIE_A_1953219_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7807/8806617/91b13b3f11d2/KBIE_A_1953219_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7807/8806617/7a8ec70b7129/KBIE_A_1953219_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7807/8806617/a9f789d0b933/KBIE_A_1953219_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7807/8806617/e1555fb706a4/KBIE_A_1953219_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7807/8806617/189b0496713f/KBIE_A_1953219_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7807/8806617/8ea6993f0d66/KBIE_A_1953219_F0006_OC.jpg

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