Rab27A promotes cellular apoptosis and ROS production by regulating the miRNA‐124‐3p/STAT3/RelA signalling pathway in ulcerative colitis

Luo, Yang; Yu, Minhao; Yan, Yuan; Zhou, Yong; Qin, Shao-Lan; Huang, Yizhou; Qin, Jun; Zhong, Ming

doi:10.1111/jcmm.15726

Cited by 24 publications

(11 citation statements)

References 40 publications

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“…Among them, 339 unique proteins existed in the former, while 243 proteins uniquely existed in the latter ( Fig. 7 B and Table 1 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 ).…”

Section: Resultsmentioning

confidence: 99%

Prmt1 upregulated by Hdc deficiency aggravates acute myocardial infarction via NETosis

Zhang

Ding

Wang

et al. 2022

Acta Pharmaceutica Sinica B

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Section: Resultsmentioning

confidence: 99%

Prmt1 upregulated by Hdc deficiency aggravates acute myocardial infarction via NETosis

Zhang

Ding

Wang

et al. 2022

Acta Pharmaceutica Sinica B

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“… 26 In multifactorial inflammatory diseases, such as ulcerative colitis, miR‐124‐3p might also regulate cellular apoptosis and reactive oxygen species production. 27 …”

Section: Discussionmentioning

confidence: 99%

The miR‐124‐3p regulates the allergic airway inflammation and remodeling in an ovalbumin‐asthmatic mouse model by inhibiting S100A4

Liu

et al. 2023

Immunity Inflam & Disease

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Objective Asthma is a chronic respiratory disease with an increasing incidence every year. microRNAs (miRNAs) have been demonstrated to have implications for asthma. However, limited information is available regarding the effect of miR‐124‐3p on this disease. Therefore, this study aimed to explore the possible effects of miR‐124‐3p and S100A4 on inflammation and epithelial–mesenchymal transition (EMT) in asthma using mouse models. Method Ovalbumin was used to induce asthmatic mouse models. Lung injury in mouse models was assessed, and the bronchoalveolar lavage fluid of mice was collected to determine the number of eosinophilic granulocytes and assess inflammation. The expression levels of miR‐124‐3p, S100A4, E‐cadherin, N‐cadherin, Snail1, vimentin, and TGF‐β1/Smad2 signaling pathway‐related proteins were measured using reverse transcription‐quantitative polymerase chain reaction (RT‐qPCR) and western blot analysis. In vitro experiments, cells were transfected with miR‐124‐3p mimics or inhibitors to test the expression of S100A4 by RT‐qPCR and western blot analysis, and the mutual binding of miR‐124‐3p and S100A4 was validated by dual‐luciferase reporter gene assay. Results Overexpression of miR‐124‐3p or inhibition of S100A4 expression attenuated bronchial mucus secretion and collagenous fibers and suppressed inflammatory cell infiltration. Additionally, upon miR‐124‐3p overexpression or S100A4 suppression, eosinophilic granulocytes were decreased, interleukin‐4 (IL‐4) and IL‐13 expression levels were reduced in the bronchoalveolar lavage fluid, serum total IgE level was reduced, and the TGF‐β1/Smad2 signaling pathway was suppressed. Mechanically, a dual‐luciferase reporter gene assay verified the binding relationship between miR‐124‐3p and S100A4. Conclusion miR‐124‐3p can negatively target S100A4 to attenuate inflammation in asthmatic mouse models by suppressing the EMT process and the TGF‐β/smad2 signaling pathway.

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“…The NF-κB pathways, including the RELA-dependent canonical pathway and the RELB-dependent noncanonical pathway, are essential for immune response modulation ( Hoesel and Schmid, 2013 ). Studies at UC also found that cellular apoptosis and ROS production could also be regulated by the RELA-related signal pathway ( Luo et al, 2020 ). In addition, phosphorylation and acetylation of RELA contribute to the transcriptional activation of various inflammatory and catabolic genes ( Kleppe et al, 2018 ; Wang et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

Therapeutic targets and pharmacological mechanisms of Coptidis Rhizoma against ulcerative colitis: Findings of system pharmacology and bioinformatics analysis

et al. 2022

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Evidence of the advantages of Coptidis Rhizoma (CR) for the treatment of ulcerative colitis (UC) is accumulating. However, research revealing the targets and molecular mechanisms of CR against UC is scarce. In this research, a bioinformatics analysis was performed to carry out the physicochemical properties and biological activities of phytochemicals in CR and analyze the binding activities, targets, biological functions and mechanisms of CR against UC. This research shows that the CR’s key phytochemicals, which are named Coptisine, Berberrubine, Berlambine, Berberine, Epiberberine, Obacunone, Worenine, Quercetin, (R)-Canadine, Magnograndiolide, Palmatine and Moupinamide, have ideal physicochemical properties and bioactivity. A total of 1,904 potential phytochemical targets and 17,995 UC-related targets are identified, and we finally acquire 233 intersection targets between key phytochemicals and disease. A protein-protein interaction network of 233 common targets was constructed; and six hub targets were acquired with a degree greater than or equal to median, namely TP53, HSP90AA1, STAT3, ESR1, MYC, and RELA. The enrichment analysis suggested that the core targets may exert an impact on anti-inflammatory, immunoregulatory, anti-oxidant and anti-fibrosis functions mainly through the PI3K/ART signaling pathway, Th17 differentiation signaling pathway, inflammatory bowel disease signaling pathway, etcetera. Also, a molecular docking analysis shows that the key phytochemicals have strong affinity for binding to the core targets. Finally, the interaction network of CR, phytochemicals, targets, GO functions, KEGG pathways and UC is constructed. This study indicates that the key phytochemicals in CR have superior drug likeness and bioactivity, and the molecular mechanism of key phytochemicals against UC may be via the signaling pathway mentioned above. The potential and critical pharmacological mechanisms provide a direction for future research.

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Rab27A promotes cellular apoptosis and ROS production by regulating the miRNA‐124‐3p/STAT3/RelA signalling pathway in ulcerative colitis

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 24 publications

References 40 publications

Prmt1 upregulated by Hdc deficiency aggravates acute myocardial infarction via NETosis

Prmt1 upregulated by Hdc deficiency aggravates acute myocardial infarction via NETosis

The miR‐124‐3p regulates the allergic airway inflammation and remodeling in an ovalbumin‐asthmatic mouse model by inhibiting S100A4

Therapeutic targets and pharmacological mechanisms of Coptidis Rhizoma against ulcerative colitis: Findings of system pharmacology and bioinformatics analysis

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