Evidence map›Paper›PMID 32815642›Full record

ArticleJournal of cellular and molecular medicine2020

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

Yang Luo, Min-Hao Yu, Ya-Ru Yan, Yong Zhou, Shao-Lan Qin, Yi-Zhou Huang, Jun Qin, Ming Zhong

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 29 citations in OpenAlex.

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  14. Acta pharmaceutica Sinica. B · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Yang LuoDepartment of Gastrointestinal Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P.R. China.
Min-Hao YuDepartment of Gastrointestinal Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P.R. China.
Ya-Ru YanDepartment of Respiratory and Critical Care Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yong ZhouDepartment of Gastrointestinal Surgery, Jiading Hospital of Traditional Chinese Medicine, Shanghai, China.
Shao-Lan QinDepartment of Gastrointestinal Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P.R. China.
Yi-Zhou HuangDepartment of Gastrointestinal Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P.R. China.
Jun QinDepartment of Gastrointestinal Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P.R. China.
Ming ZhongDepartment of Gastrointestinal Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P.R. China.ORCID 0000-0002-1869-3648
Shanghai Jiao Tong University · CNShanghai Traditional Chinese Medicine Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ulcerative colitis (UC) is a multifactorial inflammatory disease, and increasing evidence has demonstrated that the mechanism of UC pathogenesis is associated with excessive cellular apoptosis and reactive oxygen species (ROS) production. However, their function and molecular mechanisms related to UC remain unknown. In this study, Rab27A mRNA and protein were proven to be overexpressed in intestinal epithelial cells of UC patients and DSS-induced colitis mice, compared with control (P < 0.05). And Rab27A silencing inhibits inflammatory process in DSS-induced colitis mice (P < 0.05). Then, it was shown that knockdown of Rab27A suppressed apoptosis and ROS production through modulation of miR-124-3p, whereas overexpression of Rab27A promoted apoptosis and ROS production in LPS-induced colonic cells. In addition, enhanced expression of miR-124-3p attenuated apoptosis and ROS production by targeting regulation of STAT3 in LPS-induced colonic cells. Mechanistically, we found Rab27A reduced the expression and activity of miR-124-3p to activate STAT3/RelA signalling pathway and promote apoptosis and ROS production in LPS-induced colonic cells, whereas overexpression of miR-124-3p abrogated these effects of Rab27A. More importantly, animal experiments illustrated that ectopic expression of Rab27A promoted the inflammatory process, whereas overexpression of miR-124-3p might interfere with the inflammatory effect in DSS-induced colitis mice. In summary, Rab27A might modulate the miR-124-3p/STAT3/RelA axis to promote apoptosis and ROS production in inflammatory colonic cells, suggesting that Rab27A as a novel therapeutic target for the prevention and treatment of UC patients.

Indexed as

ApoptosisAdultAnimalsBase SequenceCell Line, TumorColitis, UlcerativeDextran SulfateDisease ProgressionEpithelial CellsFemaleHumansInflammationIntestinesMaleMice, Inbred C57BLMicroRNAsDextran SulfateMicroRNAsMIRN124 microRNA, humanMirn124 microRNA, mouserab27 GTP-Binding ProteinsReactive Oxygen SpeciesRNA, MessengerSTAT3 Transcription FactorTranscription Factor RelADSS-induced colitis modelmiR-124-3pRab27ASTAT3/RelA signalling pathwayulcerative colitis

Identifiers

PMID32815642
PMCPMC7576264
OpenAlexW3081159631

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.