Evidence map›Paper›PMID 23737551›Full record

ArticleScience signaling2013

TGF-β induces acetylation of chromatin and of Ets-1 to alleviate repression of miR-192 in diabetic nephropathy.

Mitsuo Kato, Varun Dang, Mei Wang, Jung Tak Park, Supriya Deshpande, Swati Kadam, Armen Mardiros, Yumei Zhan, Peter Oettgen, Sumanth Putta and 3 more

Open access · greenAbstract read
In one paragraph

Article in Science signaling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
5.1field-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, 121 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Metabolic memory: mechanisms and diseases.Signal transduction and targeted therapy · 2024
    Review
  5. Pathomechanisms of Diabetic Kidney Disease.Journal of clinical medicine · 2023
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Role of miR-379 in high-fat diet-induced kidney injury and dysfunction.American journal of physiology. Renal physiology · 2022
    Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. RT-rtPCR quantification of circulating microRNAs in plasma and serum samples from healthy domestic cats.Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians, Inc · 2021
    Article
  20. Article

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.

Mitsuo KatoDepartment of Diabetes and Division of Molecular Diabetes Research, Beckman Research Institute of the City of Hope, Duarte, CA 91010, USA. mkato@coh.org
Varun Dang
Mei Wang
Jung Tak Park
Supriya Deshpande
Swati Kadam
Armen Mardiros
Yumei Zhan
Peter Oettgen
Sumanth Putta
Hang Yuan
Linda Lanting
Rama Natarajan
City of Hope · USBeth Israel Deaconess Medical Center · US

Funding

Transforming growth factor beta1, microRNAs, lncRNA and diabetic nephropathyR01DK081705 · NIDDK · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI NATARAJAN, RAMA · 2009 to 2023
$6.1M
ROLE OF 12-LIPOXYGENASE IN DIABETIC NEPHROPATHYR01DK058191 · NIDDK · CITY OF HOPE/BECKMAN RESEARCH INSTITUTE · PI NATARAJAN, RAMA · 2001 to 2016
$5.3M
New Mechanisms in the Pathogenesis of Diabetic NephropathyR21DK076669 · NIDDK · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI NATARAJAN, RAMA · 2007 to 2008
$460k
NIDDK NIH HHS R01 DK058191NIDDK NIH HHS R01 DK081705NIDDK NIH HHS R21 DK076669
6 · The paper itself

Abstract

MicroRNAs (miRNAs), such as miR-192, mediate the actions of transforming growth factor-β1 (TGF-β) related to the pathogenesis of diabetic kidney diseases. We found that the biphasic induction of miR-192 expression by TGF-β in mouse renal glomerular mesangial cells initially involved the Smad transcription factors, followed by sustained expression that was promoted by acetylation of the transcription factor Ets-1 and of histone H3 by the acetyltransferase p300, which was activated by the serine and threonine kinase Akt. In mesangial cells from Ets-1-deficient mice or in cells in which Ets-1 was knocked down, basal amounts of miR-192 were higher than those in control cells, but sustained induction of miR-192 by TGF-β was attenuated. Furthermore, inhibition of Akt or ectopic expression of dominant-negative histone acetyltransferases decreased p300-mediated acetylation and Ets-1 dissociation from the miR-192 promoter and prevented miR-192 expression in response to TGF-β. Activation of Akt and p300 and acetylation of Ets-1 and histone H3 were increased in glomeruli from diabetic db/db mice compared to nondiabetic db/+ mice, suggesting that this pathway may contribute to diabetic nephropathy. These findings provide insight into the regulation of miRNAs through signaling-mediated changes in transcription factor activity and in epigenetic histone acetylation under normal and disease states.

Indexed as

AcetylationChromatinDiabetic NephropathiesHumansMicroRNAsTranscription FactorsTransforming Growth Factor betaChromatinMicroRNAsMIRN92 microRNA, humanTranscription FactorsTransforming Growth Factor beta

Identifiers

PMID23737551
PMCPMC3723389
OpenAlexW2119729313

What OpenQuestion holds

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LicenceTDM
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.