Evidence map›Paper›PMID 21049046›Full record

ArticlePloS one2010

miR-200b precursor can ameliorate renal tubulointerstitial fibrosis.

Shigeyoshi Oba, Shintaro Kumano, Etsu Suzuki, Hiroaki Nishimatsu, Masao Takahashi, Hajime Takamori, Masatoshi Kasuya, Yousuke Ogawa, Kenichiro Sato, Kenjiro Kimura and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 4% 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

70 citing papers in PubMed, 1 synthesis or guideline pooled it, 134 citations in OpenAlex.

  1. Guideline
  2. Review
  3. Review
  4. Article
  5. Epithelial-mesenchymal transition in tissue repair and degeneration.Nature reviews. Molecular cell biology · 2024
    Review
  6. Review
  7. Review
  8. Kidney fibrosis: from mechanisms to therapeutic medicines.Signal transduction and targeted therapy · 2023
    Review
  9. Review
  10. Article
  11. Understanding the Renal Fibrotic Process in Leptospirosis.International journal of molecular sciences · 2021
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Diverse Role of TGF-β in Kidney Disease.Frontiers in cell and developmental biology · 2020
    Review
  17. Review
  18. Article
  19. Article
  20. Non-Coding RNAs as New Therapeutic Targets in the Context of Renal Fibrosis.International journal of molecular sciences · 2019
    Review

10 more citing papers are in PubMed but not listed here.

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

13 authors at 2 institutions in 1 country.

Shigeyoshi ObaDepartment of Nephrology and Endocrinology, University of Tokyo School of Medicine, Tokyo, Japan. OBA-2IM@h.u-tokyo.ac.jp
Shintaro Kumano
Etsu Suzuki
Hiroaki Nishimatsu
Masao Takahashi
Hajime Takamori
Masatoshi Kasuya
Yousuke Ogawa
Kenichiro Sato
Kenjiro Kimura
Yukio Homma
Yasunobu Hirata
Toshiro Fujita
The University of Tokyo · JPSt. Marianna University School of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Members of the miR-200 family of micro RNAs (miRNAs) have been shown to inhibit epithelial-mesenchymal transition (EMT). EMT of tubular epithelial cells is the mechanism by which renal fibroblasts are generated. Here we show that miR-200 family members inhibit transforming growth factor-beta (TGF-beta)-induced EMT of tubular cells. Unilateral ureter obstruction (UUO) is a common model of EMT of tubular cells and subsequent tubulointerstitial fibrosis. In order to examine the role of miR-200 family members in tubulointerstitial fibrosis, their expression was investigated in the kidneys of UUO mice. The expression of miR-200 family miRNAs was increased in a time-dependent manner, with induction of miR-200b most pronounced. To clarify the effect of miR-200b on tubulointerstitial fibrosis, we injected miR-200b precursor intravenously. A single injection of 0.5 nM miR-200b precursor was sufficient to inhibit the increase of collagen types I, III and fibronectin in obstructed kidneys, and amelioration of fibrosis was confirmed by observation of the kidneys with Azan staining. miR-200 family members have been previously shown to inhibit EMT by reducing the expression of ZEB-1 and ZEB-2 which are known repressors of E-cadherin. We demonstrated that expression of ZEB-1 and ZEB-2 was increased after ureter obstruction and that administration of the miR-200b precursor reversed this effect. In summary, these results indicate that miR-200 family is up-regulated after ureter obstruction, miR-200b being strongly induced, and that miR-200b ameliorates tubulointerstitial fibrosis in obstructed kidneys. We suggest that members of the miR-200 family, and miR-200b specifically, might constitute novel therapeutic targets in kidney disease.

Indexed as

AnimalsBase SequenceBlotting, WesternDNA PrimersEpithelial-Mesenchymal TransitionFibrosisFluorescent Antibody TechniqueHumansKidney DiseasesKidney TubulesMiceMicroRNAsPolymerase Chain ReactionDNA PrimersMicroRNAsMIRN200 microRNA, human

Identifiers

PMID21049046
PMCPMC2963611
OpenAlexW2016923682

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.