LncRNA TUG1 regulates the balance of HuR and miR-29b-3p and inhibits intestinal epithelial cell apoptosis in a mouse model of ulcerative colitis

Tian, Yanhua; Wáng, Ying; Li, Fujun; Yang, Junwen; Xu, Yan; Ouyang, Ming

doi:10.1007/s13577-020-00428-5

Cited by 24 publications

(20 citation statements)

References 31 publications

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“…All mice had ad libitum access to water and food. In order to establish the dextran sodium sulfate (DSS)-induced colitis model, the mice were administered water containing 5% DSS for 7 days, and then distilled water for 3 days [ 22 ]. Meanwhile, mice in the sham group were given distilled water for 10 days.…”

Section: Methodsmentioning

confidence: 99%

Mechanism of M2 macrophage-derived extracellular vesicles carrying lncRNA MEG3 in inflammatory responses in ulcerative colitis

et al. 2021

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Ulcerative colitis (UC) is a chronic inflammatory disease of the colon. M2 macrophages possess certain anti-inflammation activity. Accordingly, the current study set out to investigate the potential mechanism of M2 macrophage-derived extracellular vesicles (M2-EVs) in UC inflammation. Firstly, mouse peritoneal macrophages were induced to M2 phenotype, and M2-EVs were isolated. , the murine model of UC was established, and the length and weight of the colon, disease activity index (DAI), apoptosis, and inflammatory response of UC mice were measured. Young adult mouse colon (YAMC) cells were induced with the help of lipopolysaccharide. LncRNA maternally expressed 3 (LncRNA MEG3), miR-20b-5p, and cAMP responsive element binding protein 1 (CREB1) expression patterns were detected in UC models. In addition, we analyzed the binding relationship among MEG3, miR-20b-5p, and CREB1. UC mice presented with shortened colon length, lightened weight, increased DAI score, enhanced apoptosis, and significant inflammatory cell infiltration, while M2-EVs reversed these trends. In vitro , M2-EVs increased UC cell viability and reduced inflammation. Mechanistic experimentation revealed that M2-EVs transferred MEG3 into YAMC cells to up-regulate MEG3 expression and promote CREB1 transcription by competitively binding to miR-20b-5p. Moreover, up-regulation of MEG3 in M2-EVs enhanced the protective effect of M2-EVs on UC cells, while over-expression of miR-20b-5p attenuated the aforementioned protective effect of M2-EVs on UC mice and cells. Collectively, our findings revealed that M2-EVs carrying MEG3 enhanced UC cell viability and reduced inflammatory responses via the miR-20b-5p/CREB1 axis, thus alleviating UC inflammation.

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Section: Methodsmentioning

confidence: 99%

Mechanism of M2 macrophage-derived extracellular vesicles carrying lncRNA MEG3 in inflammatory responses in ulcerative colitis

et al. 2021

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“…Long non-coding RNAs are families of RNAs with over 200 nucleotides. Abnormal expression of lncRNAs may function as a promoter or suppressor of UC [11][12][13]. Dysregulation of SNHG5 plays a crucial role in intestinal diseases.…”

Section: Discussionmentioning

confidence: 99%

“…The conditionally immortalized epithelial cell line of young adult mouse colon (YAMC) cell was purchased from Institute of Hematology, Chinese Academy of Medical Sciences (Tianjin, China) and cultured in complete Dulbecco's modified Eagle medium (DMEM) supplemented with 10% fetal bovine serum (FBS) (Gibco, Calif, USA) and 1% penicillin/streptomycin (Thermo Fisher, Calif, USA). YAMC cells were exposed to 10 ng/ml TNFα (10 μG; H8916-10UG; Sigma-Aldrich, NJ, USA) for 12 h to establish a model of UC in vitro [13]. si-SNHG5 1#, si-SNHG5 2#, miR-375 inhibitor, NC inhibitor, miR-375 mimic, JAK2, and the negative control or empty vector were transferred into cells using Lipofectamin TM 3000 (Life Technologies, Calif, USA).…”

Section: Cell Culture and Transfectionmentioning

confidence: 99%

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

Xuan

Zhang

et al. 2021

Bioengineered

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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 (JAK2) 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. Downregulated 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. Overexpression of miR-375 restored YAMC cellular functions. Additionally, miR-375 targeted JAK2, which was up-regulated by TNF-α treated YAMC cells. Up-regulation of JAK2 induced the dysfunction of YAMC cells. Knockdown of SNHG5 promoted the proliferation and suppressed the apoptosis of YAMC cells via regulating miR-375/JAK2 axis. Therefore, knockdown of SNHG5 may be a promising therapy for UC.

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“…For example, lncRNA TUG1 attenuated intestinal epithelial cell apoptosis and UC progression through modulating miR-29b-3p/CDK2 axis. 8 LncRNA MEG3 supplementation relieved the serve ulceration of UC rat colons via increasing IL-10 level by targeting miR-98-5p. 9 UCA1 is located in chromosome 19p13, which was first uncovered as a new lncRNA gene significantly upregulated in bladder carcinoma using RT-qPCR by Wang.…”

Section: Introductionmentioning

confidence: 95%

LncRNA UCA1 Accelerates the Progression of Ulcerative Colitis via Mediating the miR-331-3p/BRD4 Axis

Rao¹,

Shao²,

Lin³

et al. 2021

IJGM

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Background Ulcerative colitis (UC) has become one of the fastest-growing severe diseases worldwide with high morbidity. This research aimed to explore the function of lncRNA UCA1 in UC progression. Methods RT-qPCR analysis was used to examine the expression of UCA1 level in colonic mucosa tissues of UC patients. Then, fetal human cells (FHCs) were stimulated by LPS to induce inflammatory injury. CCK-8, flow cytometry and ELISA were adopted to determine the influence of UCA1 depletion on cell viability, apoptosis and pro-inflammatory factors levels in LPS-induced FHCs. The interaction between UCA1 and miR-331-3p or BRD4 was confirmed by luciferase reporter assay. The expressions of key factors involved in NF-κB pathway were assessed by Western blotting. Results LncRNA UCA1 level was elevated in colonic mucosa tissues of UC patients. LPS stimulation restrained cell viability and promoted the apoptosis and inflammatory factors levels, thus inducing FHCs inflammatory injury, while these effects were partially abolished by UCA1 knockdown. Moreover, it was found that UCA1 silence improved LPS-triggered cell injury via miR-331-3p. In addition, BRD4 was directly targeted by miR-331-3p, and BRD4 deficiency neutralized the effects of miR-331-3p repression on LPS-triggered injury in LPS-treated FHCs. Conclusion Our data determined that UCA1 knockdown attenuated UC development via targeting the miR-331-3p/BRD4/NF-κB pathway.

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LncRNA TUG1 regulates the balance of HuR and miR-29b-3p and inhibits intestinal epithelial cell apoptosis in a mouse model of ulcerative colitis

Cited by 24 publications

References 31 publications

Mechanism of M2 macrophage-derived extracellular vesicles carrying lncRNA MEG3 in inflammatory responses in ulcerative colitis

Mechanism of M2 macrophage-derived extracellular vesicles carrying lncRNA MEG3 in inflammatory responses in ulcerative colitis

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

LncRNA UCA1 Accelerates the Progression of Ulcerative Colitis via Mediating the miR-331-3p/BRD4 Axis

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