METTL14 regulates inflammation in ulcerative colitis via the lncRNA DHRS4-AS1/miR-206/A3AR axis DOI Creative Commons

Weiyun Wu,

Xiaowen Li,

Zhuliang Zhou

et al.

Cell Biology and Toxicology, Journal Year: 2024, Volume and Issue: 40(1)

Published: Nov. 11, 2024

As a chronic inflammatory bowel disease, the pathogenesis of ulcerative colitis (UC) has not been fully elucidated. N6-methyladenosine (m6A) modification, observed in various RNAs, is implicated diseases. Methyltransferase-like 14 (METTL14) major subunit methyltransferase complex catalyzing m6A modifications. Here, we designated to examine regulatory effects and mechanisms METTL14 on long non-coding RNA (lncRNA) during UC progression. knockdown decreased cell viability, promoted apoptosis, increased cleaved PARP Caspase-3 levels, while reducing Bcl-2 levels. also led significant increase NF-κB pathway activation cytokine production Caco-2 cells treated with TNF-α. Moreover, suppression aggravated colonic damage inflammation our dextran sulfate sodium (DSS)-induced murine model. silencing suppressed DHRS4-AS1 expression by modification transcripts. Furthermore, mitigated injury targeting miR-206/adenosine A3 receptor (A3AR) axis. overexpression counteracted enhancing impact TNF-α-induced cells. In conclusion, findings suggest that protects against via regulating DHRS4-AS1/miR-206/A3AR axis, thus representing potential therapeutic target for UC.

Language: Английский

Anti-TNFα in inflammatory bowel disease: from originators to biosimilars DOI Creative Commons
Zhen Zeng, Hao Lin, Mingshan Jiang

et al.

Frontiers in Pharmacology, Journal Year: 2024, Volume and Issue: 15

Published: July 24, 2024

The introduction of anti-tumor necrosis factor α (TNFα) biologics significantly innovated inflammatory bowel disease (IBD) treatment and increased medical costs. recent expiration patents some anti-TNFα (such as infliximab adalimumab) facilitated the development biosimilars. Comparable pharmacokinetic, efficacy, safety, immunogenicity profiles between originators biosimilars were demonstrated in different studies. Anti-TNFα hold promise for reducing high cost increasing patient access to biologics. In this review, we outline current data on use patients with IBD, a focus adalimumab potential benefits, challenges, future directions are also discussed review.

Language: Английский

Citations

3
Regulation of Bacteroides acidifaciens by the aryl hydrocarbon receptor in IL-22-producing immune cells has sex-dependent consequential impact on colitis DOI Creative Commons
Chandani Mitchell,

Shanieka Staley,

Michal Claire Williams

et al.

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: Aug. 20, 2024

Colitis is an inflammatory bowel disease (IBD) characterized by immune cell dysregulation and alterations in the gut microbiome. In our previous report, we showed a natural product cruciferous vegetables ligand of aryl hydrocarbon receptor (AhR), indole-3-carbinol (I3C), was able to reduce colitis-induced severity microbial dysbiosis interleukin-22 (IL-22) dependent manner.

Language: Английский

Citations

3
Suppression of MyD88 disturbs gut microbiota and activates NLRs pathway hence fails to ameliorate DSS-induced colitis DOI Creative Commons
Junhua Li, Yu Chen, Zhenghao Ye

et al.

Precision Clinical Medicine, Journal Year: 2024, Volume and Issue: 7(2)

Published: May 1, 2024

Myeloid differentiation factor 88 (MyD88) is the core adaptor for Toll-like receptors defending against microbial invasion and initiating a downstream immune response during microbiota-host interaction. However, role of MyD88 in pathogenesis inflammatory bowel disease controversial. This study aims to investigate impact on intestinal inflammation underlying mechanism.

Language: Английский

Citations

2
Expression profile of Toll-like receptors and cytokines in the cecal tonsil of chickens challenged with Eimeria tenella DOI
Danni Wang, Qian Zhang, Zhen Zhang

et al.

Parasitology Research, Journal Year: 2024, Volume and Issue: 123(10)

Published: Oct. 1, 2024

Language: Английский

Citations

0
METTL14 regulates inflammation in ulcerative colitis via the lncRNA DHRS4-AS1/miR-206/A3AR axis DOI Creative Commons

Weiyun Wu,

Xiaowen Li,

Zhuliang Zhou

et al.

Cell Biology and Toxicology, Journal Year: 2024, Volume and Issue: 40(1)

Published: Nov. 11, 2024

As a chronic inflammatory bowel disease, the pathogenesis of ulcerative colitis (UC) has not been fully elucidated. N6-methyladenosine (m6A) modification, observed in various RNAs, is implicated diseases. Methyltransferase-like 14 (METTL14) major subunit methyltransferase complex catalyzing m6A modifications. Here, we designated to examine regulatory effects and mechanisms METTL14 on long non-coding RNA (lncRNA) during UC progression. knockdown decreased cell viability, promoted apoptosis, increased cleaved PARP Caspase-3 levels, while reducing Bcl-2 levels. also led significant increase NF-κB pathway activation cytokine production Caco-2 cells treated with TNF-α. Moreover, suppression aggravated colonic damage inflammation our dextran sulfate sodium (DSS)-induced murine model. silencing suppressed DHRS4-AS1 expression by modification transcripts. Furthermore, mitigated injury targeting miR-206/adenosine A3 receptor (A3AR) axis. overexpression counteracted enhancing impact TNF-α-induced cells. In conclusion, findings suggest that protects against via regulating DHRS4-AS1/miR-206/A3AR axis, thus representing potential therapeutic target for UC.

Language: Английский

Citations

0