Evidence map›Paper›PMID 21465537›Full record

ArticleJournal of cellular biochemistry2011

Histone deacetylase 1/2 mediates proliferation of renal interstitial fibroblasts and expression of cell cycle proteins.

Maoyin Pang, Li Ma, Na Liu, Murugavel Ponnusamy, Ting C Zhao, Haidong Yan, Shougang Zhuang

Open access · greenAbstract read
In one paragraph

Article in Journal of cellular biochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.4field-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

34 citing papers in PubMed, 60 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Histone deacetylases and their inhibitors in kidney diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Critical review of non-histone human substrates of metal-dependent lysine deacetylases.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Integrative analysis of miRNA and mRNA paired expression profiling of primary fibroblast derived from diabetic foot ulcers reveals multiple impaired cellular functions.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society · 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

7 authors at 4 institutions in 2 countries.

Maoyin PangDepartment of Medicine, Brown University School of Medicine, Rhode Island Hospital, Providence, Rhode Island 02903, USA.
Li Ma
Na Liu
Murugavel Ponnusamy
Ting C Zhao
Haidong Yan
Shougang Zhuang
Rhode Island Hospital · USBrown University · USRoger Williams Medical Center · USShanghai East Hospital · CN

Funding

Histone deacetylases as novel therapeutic targets for kidney fibrosisR01DK085065 · NIDDK · RHODE ISLAND HOSPITAL · PI ZHUANG, SHOUGANG · 2010 to 2017
$2.8M
Dedifferentiation Following Renal Cell InjuryR01DK071997 · NIDDK · RHODE ISLAND HOSPITAL · PI ZHUANG, SHOUGANG · 2006 to 2009
$1.1M
NIDDK NIH HHS DK-071997NIDDK NIH HHS DK-085065NIDDK NIH HHS R01 DK071997NIDDK NIH HHS R01 DK085065
6 · The paper itself

Abstract

We recently reported that the histone deacetylase (HDAC) activity is required for activation of renal interstitial fibroblasts. In this study, we further examined the role of HDACs, in particular, HDAC1 and HDAC2, in proliferation of cultured rat renal interstitial fibroblasts (NRK-49F) and expression of cell cycle proteins. Inhibition of HDAC activity with trichostatin A (TSA), blocked cell proliferation, decreased expression of Cyclin D1, a positive cell cycle regulator, and increased expression of p27 and p57, two negative cell cycle regulators. Silencing either HDAC1 or HDAC2 with siRNA also significantly inhibited cell proliferation, decreased expression of Cyclin D1, and increased expression of p57. However, down-regulation of HDAC2, but not HDAC1 resulted in increased expression of p27. Furthermore, HDAC1 and HDAC2 down-regulation was associated with dephosphorylation and hyperacetylation of STAT3 (Signal transducer and activator of transcription 3). Blockade of STAT3 with S3I-201 or siRNA decreased renal fibroblast proliferation. Finally, mouse embryonic fibroblasts (MEFs) lacking STAT3 reduced the inhibitory effect of TSA on cell proliferation, add-back of wild type STAT3 to STAT3(-/-) MEFs restored the effect of TSA. Collectively, our results reveal an important role of HDAC1 and HDAC2 in regulating proliferation of renal interstitial fibroblasts, expression of cell cycle proteins and activation of STAT3. Further, STAT3 mediates the proliferative action of HDACs.

Indexed as

Cell ProliferationAnimalsCell Cycle ProteinsCells, CulturedFibroblastsHistone Deacetylase 1Histone Deacetylase 2Histone Deacetylase InhibitorsHydroxamic AcidsKidneyMiceMice, KnockoutRatsSTAT3 Transcription FactorCell Cycle ProteinsHdac1 protein, mouseHdac1 protein, ratHdac2 protein, mouseHdac2 protein, ratHistone Deacetylase 1Histone Deacetylase 2Histone Deacetylase InhibitorsHydroxamic AcidsStat3 protein, mouseStat3 protein, ratSTAT3 Transcription Factortrichostatin A

Identifiers

PMID21465537
PMCPMC4626014
OpenAlexW2061446762

What OpenQuestion holds

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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.