Evidence map›Paper›PMID 31949659›Full record

ArticleInternational journal of clinical and experimental pathology2018

MicroRNA-142-5p facilitates the pathogenesis of ulcerative colitis by regulating SOCS1.

Jing Han, Yawei Li, Hong Zhang, Jinbo Guo, Xing Wang, Yaxing Kang, Yuxin Luo, Mengyao Wu, Xiaolan Zhang

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.6field-weighted citation impact, top 38% 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

10 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. MiR-222-3p Aggravates the Inflammatory Response by Targeting SOCS1 to Activate STAT3 Signaling in Ulcerative Colitis.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2022
    Article
  6. Review
  7. Article
  8. Article
  9. Article
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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

9 authors at 1 institution in 1 country.

Jing HanDepartment of Gastroenterology, The East Branch of The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology Shijiazhuang, China.
Yawei LiDepartment of Cardiology, The Third Hospital of Shijiazhuang Shijiazhuang, Hebei, China.
Hong ZhangDepartment of Gastroenterology, The East Branch of The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology Shijiazhuang, China.
Jinbo GuoDepartment of Gastroenterology, The East Branch of The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology Shijiazhuang, China.
Xing WangDepartment of Gastroenterology, The East Branch of The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology Shijiazhuang, China.
Yaxing KangDepartment of Gastroenterology, The East Branch of The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology Shijiazhuang, China.
Yuxin LuoDepartment of Gastroenterology, The East Branch of The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology Shijiazhuang, China.
Mengyao WuDepartment of Gastroenterology, The East Branch of The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology Shijiazhuang, China.
Xiaolan ZhangDepartment of Gastroenterology, The East Branch of The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology Shijiazhuang, China.
Hebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIncreasing evidence suggests that abnormal levels of microRNAs (miRNAs) are associated with ulcerative colitis (UC). It has been demonstrated that microRNA (miR)-142-5p was upregulated in UC patients. However, it remains unclear what the role of miR-142-5p is in UC.

methodsSamples from patients with active UC and healthy controls were performed with miRNA microarray to identify miRNAs involved in the pathogenesis of UC. The results of quantitative RT-PCR verified that miR-142-5p was upregulated in UC patients. Meanwhile, the decreased expression of suppressor of cytokine signaling 1 (SOCS1) was also detected at mRNA and protein levels. The regulatory effect of miR-142-5p on SOCS1 was evaluated by luciferase reporter assay. Levels of IL-6 or IL-8 were detected by quantitative RT-PCR or enzyme-linked immunosorbent assay in HT-29 cells to evaluate the roles of SOCS1 or miR-142-5p in the progression of UC.

resultsThe expression level of miR-142-5p was significantly upregulated and inversely correlated with SOCS1. Luciferase experiments showed that miR-142-5p interfered with the expression of SOCS1 by directly targeting its 3'-UTR. Furthermore, the level of miR-142-5p plays an important role in the secretion of IL-6 and IL-8. Moreover, lost function of SOCS1 reversed the miR-142-5p inhibitory effect.

conclusionsThese results indicate that miR-142-5p improved the intestinal inflammation of active-UC patients by downregulating SOCS1 expression and increasing the cytokines IL-6 and IL-8 secretion.

Indexed as

microRNAsmiR-142-5pSOCS1ulcerative colitis

Identifiers

PMID31949659
PMCPMC6963094
OpenAlexW3012692477

What OpenQuestion holds

Textmetadata
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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.