Loss of miR-24-3p promotes epithelial cell apoptosis and impairs the recovery from intestinal inflammation

Soroosh, Artin; Fang, Kai; Hoffman, Jill M.; Law, Ivy Ka Man; Videlock, Elizabeth J.; Lokhandwala, Zulfiqar A.; Zhao, Jonathan J; Hamidi, Sepehr; Padua, David; Frey, Mark R.; Pothoulakis, Charalabos; Rankin, Carl R.

doi:10.1038/s41419-021-04463-4

Cited by 6 publications

(6 citation statements)

References 37 publications

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“…Loss of miR-24-3p promotes epithelial cell apoptosis and impairs the recovery from intestinal inflammation. 38 MiR-200b-3p alleviates TNF-α-induced apoptosis and inflammation of intestinal epithelial cells and ulcerative colitis progression in rats. 39 Here, we identified that miR-222-3p has a binding site for SOCS1 by bioinformatics analysis and confirmed their targeted relationship.…”

Section: Discussionmentioning

confidence: 98%

MiR-222-3p Aggravates the Inflammatory Response by Targeting SOCS1 to Activate STAT3 Signaling in Ulcerative Colitis

Xia¹,

Bo²,

Ding³

et al. 2022

Turk J Gastroenterol

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Background: Ulcerative colitis is characterized by relapsing inflammation in the gastrointestinal tract with limited treatment options. The aim of the present study was to assess the anti-inflammatory effect of Suppressor of cytokine signaling ( SOCS1 ) on lipopolysaccharide-stimulated RAW264.7 cells and to investigate its potential mechanisms. Methods: The in vitro ulcerative colitis model was established by using lipopolysaccharide-stimulated RAW264.7 cells. Western blotting was used to detect the protein expression levels of SOCS1 , JAK2 , STAT3 , and VDR . Reverse transcription-quantitative polymerase chain reaction was used to measure the mRNA expression of SOCS1 , miR-222-3p, and VDR . An enzyme-linked immunosorbent assay was performed to measure the levels of inflammatory cytokines. A luciferase assay assessed the binding of SOCS1 to miR-222-3p. A total of 15 patients with ulcerative colitis and 18 healthy controls were recruited. The expression levels of SOCS1 and miR-222-3p in the colonic mucosa tissues of patients with ulcerative colitis and healthy controls were determined by reverse transcription-quantitative polymerase chain reaction. Results: SOCS1 upregulation inhibited the lipopolysaccharide-induced inflammation in RAW264.7 cells. SOCS1 was confirmed to be targeted by miR-222-3p. Silencing SOCS1 significantly abolished the inhibitory effects of miR-222-3p downregulation on inflammation. MiR-222-3p activated STAT3 signaling and reduced VDR expression by targeting SOCS1 in lipopolysaccharide-treated RAW264.7 cells. Additionally, miR-222-3p expression was upregulated in ulcerative colitis patients ( P = 5.16E−10), while SOCS1 ( P = 2.75E−10) and VD R ( P = 52.5E−9) expression was downregulated in ulcerative colitis patients. Endoscopic scores (UCEIS) revealed significant positive correlation with miR-222-3p and negative correlation with SOCS1 and VDR . Conclusion: MiR-222-3p targets SOCS1 to aggravate the inflammatory response by suppressing VDR and activating STAT3 signaling in ulcerative colitis.

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Section: Discussionmentioning

confidence: 98%

MiR-222-3p Aggravates the Inflammatory Response by Targeting SOCS1 to Activate STAT3 Signaling in Ulcerative Colitis

Xia¹,

Bo²,

Ding³

et al. 2022

Turk J Gastroenterol

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“…The dysregulation of MIR4435-2HG in UC might play a key role in the inflammatory process and has been shown to be associated with CRC [ 37 , 42 , 43 ]. MIR4435-2HG is correlated with the expression of B cell lymphoma 2 (Bcl-2)-interacting protein (BCL2L11), which is associated with an increase in apoptosis resistance, resulting in impaired epithelial cell turnover [ 44 ]. In addition, BCL2L11 also plays a major role in immune tolerance in UC [ 45 ].…”

Section: Discussionmentioning

confidence: 99%

Methylation-Regulated Long Non-Coding RNA Expression in Ulcerative Colitis

Fenton,

Ray,

Meng

et al. 2023

IJMS

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Long non-coding RNAs (lncRNAs) have been shown to play a role in the pathogenesis of ulcerative colitis (UC). Although epigenetic processes such as DNA methylation and lncRNA expression are well studied in UC, the importance of the interplay between the two processes has not yet been fully explored. It is, therefore, believed that interactions between environmental factors and epigenetics contribute to disease development. Mucosal biopsies from 11 treatment-naïve UC patients and 13 normal controls were used in this study. From each individual sample, both whole-genome bisulfite sequencing data (WGBS) and lncRNA expression data were analyzed. Correlation analysis between lncRNA expression and upstream differentially methylated regions (DMRs) was used to identify lncRNAs that might be regulated by DMRs. Furthermore, proximal protein-coding genes associated with DMR-regulated lncRNAs were identified by correlating their expression. The study identified UC-associated lncRNAs such as MIR4435-2HG, ZFAS1, IL6-AS1, and Pvt1, which may be regulated by DMRs. Several genes that are involved in inflammatory immune responses were found downstream of DMR-regulated lncRNAs, including SERPINB1, CCL18, and SLC15A4. The interplay between lncRNA expression regulated by DNA methylation in UC might improve our understanding of UC pathogenesis.

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“…To explore the anti-inflammatory effect of ATR on RAW264.7 cells, alterations in TNF-α, IL-6, SOD, MDA, and GSH were examined using ELISA, and ROS were examined using flow cytometry. The results depicted in Figure 2A,B demonstrate that ATR at various concentrations (1,5,25, and 125 μg/mL) significantly inhibited the secretion of TNF-α in LPS-induced RAW264.7 inflammatory cells (p < 0.05). However, only a high dosage (125 g/mL) of ATR was able to suppress the proinflammatory cytokine IL-6 in a doseindependent manner.…”

Section: Atr Inhibits Lps-induced Inflammatory Reactions In Raw2647 C...mentioning

confidence: 90%

“…Ulcerative colitis (UC) is a chronic inflammatory disease of the colon and rectum [1], characterized by a course of relapsing and remitting symptoms. The defining features of UC encompass bloody diarrhea, along with the occurrence of rectal urgency and tenesmus [2].…”

Section: Introductionmentioning

confidence: 99%

Atractylone in the Atractylodes macrocephala Rhizoma Essential Oil and Its Anti-Inflammatory Activity

Li,

He,

Wang

et al. 2023

Molecules

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The aim of this study was to conduct a screening of potential therapeutic compounds found in the Atractylodes macrocephala rhizoma essential oil (AO) and explore its mechanism of action in the treatment of ulcerative colitis (UC). An inflammation cell model was employed in conjunction with phospho-antibody array technology to explore potential therapeutic compounds of AO and their anti-inflammatory and antioxidant effects. Furthermore, we assessed their efficacy and mechanisms of action in treating dextran sulfate sodium (DSS)-induced colitis in mice. Via the screening process, we identified atractylone (ATR) as the primary active compound in AO. It has been demonstrated that ATR can both decrease the levels of tumor necrosis factor (TNF)-α and reactive oxygen species (ROS) and increase the expression of adhesion proteins such as claudin, ZO-1, and occludin in vitro. Moreover, ATR has been shown to improve UC symptoms in vivo. Via a non-targeted metabolomics analysis of colon tissue, we identified 57 distinct metabolites that responded to ATR treatment. Subsequent analysis of the metabolic pathways revealed that the action of ATR was primarily focused on the amino acid metabolism pathway. In summary, ATR may alleviate the symptoms of UC by regulating multiple signaling pathways. Additionally, ATR has a comprehensive function in anti-inflammation, antioxidative stress, and intestinal injury reduction.

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Loss of miR-24-3p promotes epithelial cell apoptosis and impairs the recovery from intestinal inflammation

Cited by 6 publications

References 37 publications

MiR-222-3p Aggravates the Inflammatory Response by Targeting SOCS1 to Activate STAT3 Signaling in Ulcerative Colitis

MiR-222-3p Aggravates the Inflammatory Response by Targeting SOCS1 to Activate STAT3 Signaling in Ulcerative Colitis

Methylation-Regulated Long Non-Coding RNA Expression in Ulcerative Colitis

Atractylone in the Atractylodes macrocephala Rhizoma Essential Oil and Its Anti-Inflammatory Activity

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