Circular RNA_0001187 participates in the regulation of ulcerative colitis development via upregulating myeloid differentiation factor 88

Ouyang, Wei; Wu, Min; Wu, Anshan; Xiao, Heng

doi:10.1080/21655979.2022.2077572

Cited by 9 publications

(5 citation statements)

References 39 publications

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“…26 Circ_0001187 knockdown could repress oxidative stress, inflammation and apoptosis in TNFα-induced UC cell models. 27 In addition, circAtp9b, which was overexpressed in UC patients, had been shown to promote LPS-induced colonic epithelial cell apoptosis. 28 These results confirm the importance of circRNA in regulating UC process.…”

Section: Discussionmentioning

confidence: 99%

“…Upregulation of circHECTD1 could promote autophagy to suppress LPS‐induced Caco2 cell inflammation and DSS‐induced colonic injury 26 . Circ_0001187 knockdown could repress oxidative stress, inflammation and apoptosis in TNF‐α‐induced UC cell models 27 . In addition, circAtp9b, which was overexpressed in UC patients, had been shown to promote LPS‐induced colonic epithelial cell apoptosis 28 .…”

Section: Discussionmentioning

confidence: 99%

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CircSOD2: Disruption of intestinal mucosal barrier function in ulcerative colitis by regulating the miR‐378g/Snail1 axis

Ye,

Zhang,

Peng

et al. 2024

J of Gastro and Hepatol

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Background and AimCircular RNA (circRNA) has been found to mediate ulcerative colitis (UC) progression by regulating intestinal mucosal barrier function. However, the role of circSOD2 in UC process and its underlying molecular mechanism still need to be further elucidated.MethodsLipopolysaccharide (LPS)‐induced Caco2 cells were used to mimic UC cell models. CircSOD2, miR‐378g, and Snail1 levels were determined by quantitative real‐time PCR. Cell viability was detected using MTT assay, and inflammatory cytokine levels were measured using ELISA. The intestinal mucosal barrier function was evaluated by testing transepithelial electrical resistance and fluorescein isothiocyanate (FITC)‐dextran permeability. Snail1 and tight junction‐related markers (Zo‐1 and Claudin2) protein levels were examined using western blot. The interaction between miR‐378g and circSOD2 or Snail1 was confirmed by dual‐luciferase reporter assay. Dextran sulfate sodium (DSS) was used to induce UC rat models in vivo.ResultsCircSOD2 was overexpressed in UC patients, and its knockdown significantly increased cell viability, transepithelial electrical resistance, and tight junction‐related protein expression, while reduced inflammation cytokine levels and the permeability of FITC‐dextran in LPS‐induced Caco2 cells. In terms of mechanism, circSOD2 sponged miR‐378g to positively regulate Snail1 expression. MiR‐378g inhibitor reversed the effect of circSOD2 knockdown on intestinal mucosal barrier injury and Snail1 expression in LPS‐induced Caco2 cells. In DSS‐induced UC rat models, circSOD2 knockdown also could repair the intestinal mucosal barrier injury through regulating miR‐378g/Snail1 axis.ConclusionCircSOD2 could destroy intestinal mucosal barrier function in LPS‐induced Caco2 cells and DSS‐induced UC rats by miR‐378g/Snail1 axis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

CircSOD2: Disruption of intestinal mucosal barrier function in ulcerative colitis by regulating the miR‐378g/Snail1 axis

Ye,

Zhang,

Peng

et al. 2024

J of Gastro and Hepatol

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“…Normal human colonic epithelial cells (NCM460, passages 3-5) were purchased from Jihe Biotechnology Co, Ltd (Shanghai, China) and maintained in Roswell Park Memorial Institute-1640 (RPMI-1640) at 37°C with 5% CO 2 . NCM460 cells were treated with 10 ng/mL of TNF-α for 12 h to mimic UC-like cell inflammation and injury in vitro (18,19).…”

Section: Cell Culture and Treatmentmentioning

confidence: 99%

Circ_0085323 Silencing Inhibits TNF-Α-Induced Normal Human Colonic Epithelial Cell Inflammation and Apoptosis Through the Mir-495-3p/Traf3 Axis

An,

Yang,

Tao

et al. 2023

Shock

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Background: Previous data have suggested the involvement of circular RNA (circRNA) in ulcerative colitis (UC) development. However, the role and mechanism of circ_0085323 in UC occurrence have not been reported. Methods: Normal human colonic epithelial cells (NCM460) were treated with TNF-α to simulate UC-like cell inflammation and injury in vitro. The expression of circ_0085323, microRNA-495-3p (miR-495-3p), and TNF receptor–associated factor 3 (TRAF3) was detected by quantitative real-time polymerase chain reaction. Protein expression was checked by western blotting analysis. Cell viability, cell proliferation, and cell apoptosis were investigated by cell counting kit-8 assay, 5-ethynyl-29-deoxyuridine assay, and flow cytometry analysis, respectively. IL-1β, IL-6, and IL-8 production were analyzed by enzyme-linked immunosorbent assays. Lactate dehydrogenase activity was assessed by a lactate dehydrogenase activity detection assay. The interactions among circ_0085323, miR-495-3p, and TRAF3 were identified by dual-luciferase reporter assay and RNA immunoprecipitation assay. Results: Circ_0085323 was overexpressed in the colonic mucosal tissues of UC patients and TNF-α–stimulated NCM460 cells. Circ_0085323 knockdown relieved TNF-α–induced inhibitory effect on the proliferation of NCM460 cells and promoting effects on cell apoptosis and inflammation. Circ_0085323 acted as a miR-495-3p sponge, and the effects of circ_0085323 silencing on TNF-α–induced NCM460 cell injury were attenuated by decreasing miR-495-3p expression. TRAF3 was targeted by miR-495-3p, and circ_0085323 combined with miR-495-3p to regulate TRAF3. TRAF3 depletion not only alleviated TNF-α–induced NCM460 cell damage but also partially revoked the effect of circ_0085323 silencing combined with miR-495-3p depletion on TNF-α–induced NCM460 cell injury. Conclusions: Circ_0085323 knockdown ameliorated TNF-α–induced NCM460 cell injury by regulating the miR-495-3p/TRAF3 axis, which suggested that circ_0085323 might be a therapeutic target for UC.

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“…The level of circ_0001187 was increased in colonic mucosa from UC patients ( 102 ). Circ_0001187 acted as a sponge of miR-1236-3p which targeted MYD88.…”

Section: Roles Of Circrnas In Ibdmentioning

confidence: 99%

Circular RNAs in inflammatory bowel disease

Lun,

Guo,

et al. 2023

Front. Immunol.

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Inflammatory bowel disease (IBD) is a term encompassing a few chronic inflammatory disorders that leads to damage of the intestinal tract. Although much progress has been made in understanding the pathology of IBD, the precise pathogenesis is not completely understood. Circular RNAs (circRNAs) are single-stranded, covalently closed, endogenous molecules in eukaryotes with a variety of biological functions. CircRNAs have been shown to have regulatory effects in many diseases, such as cancer, cardiovascular disease, and neurological disorders. CircRNAs have also been found to play important roles in IBD, and although they are not sufficiently investigated in the context of IBD, a few circRNAs have been identified as potential biomarkers for the diagnosis and prognosis of IBD and as potential therapeutic targets for IBD. Herein, we survey recent progress in understanding the functions and roles of circRNAs in IBD and discuss their potential clinical applications.

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Circular RNA_0001187 participates in the regulation of ulcerative colitis development via upregulating myeloid differentiation factor 88

Cited by 9 publications

References 39 publications

CircSOD2: Disruption of intestinal mucosal barrier function in ulcerative colitis by regulating the miR‐378g/Snail1 axis

CircSOD2: Disruption of intestinal mucosal barrier function in ulcerative colitis by regulating the miR‐378g/Snail1 axis

Circ_0085323 Silencing Inhibits TNF-Α-Induced Normal Human Colonic Epithelial Cell Inflammation and Apoptosis Through the Mir-495-3p/Traf3 Axis

Circular RNAs in inflammatory bowel disease

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