Evidence map›Paper›PMID 26259828›Full record

ArticleScientific reports2015

miR-744 enhances type I interferon signaling pathway by targeting PTP1B in primary human renal mesangial cells.

Xiaoyan Zhang, Xiao Han, Yuanjia Tang, Yanfang Wu, Bo Qu, Nan Shen

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

20 citing papers in PubMed, 31 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Type I IFN in Glomerular Disease: Scarring beyond the STING.International journal of molecular sciences · 2024
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. MicroRNAs as Master Regulators of Glomerular Function in Health and Disease.Journal of the American Society of Nephrology : JASN · 2017
    Review
  18. Article
  19. Review
  20. TLR9 expression is required for the development of cigarette smoke-induced emphysema in mice.American journal of physiology. Lung cellular and molecular physiology · 2016
    Article
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

6 authors at 3 institutions in 1 country.

Xiaoyan ZhangShanghai Institute of Rheumatology, Department of Rheumatology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Xiao HanInstitute of Health Sciences, Shanghai Institutes for Biological Sciences (SIBS) &Shanghai Jiao Tong University School of Medicine (SJTUSM), Chinese Academy of Sciences (CAS), Shanghai, China.
Yuanjia TangShanghai Institute of Rheumatology, Department of Rheumatology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Yanfang WuShanghai Institute of Rheumatology, Department of Rheumatology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Bo QuShanghai Institute of Rheumatology, Department of Rheumatology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Nan Shen1] Shanghai Institute of Rheumatology, Department of Rheumatology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China [2] Institute of Health Sciences, Shanghai Institutes for Biological Sciences (SIBS) &Shanghai Jiao Tong University School of Medicine (SJTUSM), Chinese Academy of Sciences (CAS), Shanghai, China [3] Division of Rheumatology and the Center for Autoimmune Genomics and Etiology (CAGE),Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, United States of America.
Shanghai Jiao Tong University · CNRenji Hospital · CNShanghai Institutes for Biological Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal mesangial cells (RMCs) constitute a population of cells in glomerular mesangium. Inflammatory cytokines produced by RMCs play a vital role in renal inflammation. miRNAs are key regulators of inflammatory cytokine expression. The abnormal expression of renal miRNAs and the consequent changes in inflammatory signal transduction are closely associated with renal inflammation. However, our knowledge of the functions of renal miRNAs is still limited. In this study, we investigated the role of miR-744 in type I interferon (IFN) signaling pathway in primary human RMCs. We show that overexpression of miR-744 enhances IFN-induced CCL2, CCL5, CXCL10, and IL6 expression specifically in RMCs. We found that the activation of TYK2, STAT1 and STAT3 was significantly enhanced by miR-744. miR-744 also enhanced the activation of non-classical signal components, such as ERK and p38. We then identified PTP1B, a ubiquitously expressed phosphatase, as the target of miR-744 that is responsible for enhancing type I IFN response. Finally, miR-744 expression was induced by type I IFN in RMCs. Collectively, our data indicate that by targeting PTP1B, miR-744 plays a feed-forward role in regulating type I IFN signaling pathway. These findings give us new insights into the functions of renal miRNAs in regulating important signaling pathways.

Indexed as

CytokinesGene Expression RegulationHumansImmunity, InnateInflammationInterferon Type IKidneyMesangial CellsMicroRNAsPrimary Cell CultureProtein Tyrosine Phosphatase, Non-Receptor Type 1Signal TransductionCytokinesInterferon Type IMicroRNAsMIRN744 microRNA, humanProtein Tyrosine Phosphatase, Non-Receptor Type 1PTPN1 protein, human

Identifiers

PMID26259828
PMCPMC4531339
OpenAlexW1193814196

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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.