Evidence map›Paper›PMID 24460719›Full record

ArticleCell proliferation2013

Role of histone deacetylases in regulation of phenotype of ovine newborn pulmonary arterial smooth muscle cells.

Q Yang, M J Dahl, K H Albertine, R Ramchandran, M Sun, J U Raj

Open access · greenAbstract read
In one paragraph

Article in Cell proliferation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

22 citing papers in PubMed, 30 citations in OpenAlex.

  1. The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026
    Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Targeting Bromodomain-Containing Protein 9 in Human Uterine Fibroid Cells.Reproductive sciences (Thousand Oaks, Calif.) · 2025
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Extracellular superoxide dismutase and its role in cancer.Free radical biology & medicine · 2017
    Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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.

Q YangDepartment of Pediatrics, University of Illinois at Chicago, Chicago, IL, 60612, USA.
M J Dahl
K H Albertine
R Ramchandran
M Sun
J U Raj
University of Illinois Chicago · USUniversity of Utah · USUniversity of Illinois Hospital & Health Sciences System · US

Funding

Mechanisms of cGMP-Mediated Vasodilation in Perinatal LungR01HL059435 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI RAJ, J. USHA · 1998 to 2010
$3.9M
Functional Heterogeneity of Pulmonary Arteries and VeinsR01HL075187 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI RAJ, J. USHA · 2003 to 2011
$3.8M
Epigenetics participate in neonatal CLDR01HL110002 · NHLBI · UNIVERSITY OF UTAH · PI ALBERTINE, KURT H · 2011 to 2015
$2.3M
Role of microRNA-17-92 and PDLIM5 Signaling in Pulmonary Arterial HypertensionR01HL123804 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI RAJ, J. USHA, ZHOU, GUOFEI · 2015 to 2018
$1.6M
NHLBI NIH HHS R01 HL059435NHLBI NIH HHS R01 HL075187NHLBI NIH HHS R01 HL110002NHLBI NIH HHS R01 HL123804
6 · The paper itself

Abstract

objectivePulmonary arterial hypertension, characterized by pulmonary vascular remodelling and vasoconstriction, is associated with excessive proliferative changes in pulmonary vascular walls. However, the role of HDACs in the phenotypic alteration of pulmonary arterial smooth muscle cells (PASMC) is largely unknown. MATERIAL AND

methodsPulmonary arterial smooth muscle cells were isolated from newborn sheep. Cell cycle analysis was performed by flow cytometry. mRNA and protein expression were measured by real-time PCR and Western blot analysis. Wound-healing scratch assay was used to measure cell migration. Contractility of newborn PASMCs was determined by gel contraction assay. Chromatin immunoprecipitation was used to examine histone modifications along the p21 promoter region. Global DNA methylation was measured by liquid chromatography-mass spectroscopy.

resultsInhibition of class I and class II HDACs by apicidin and HDACi VIII suppressed proliferation of newborn PASMC and induced cell cycle arrest in G1 phase. Acetyl H3 levels were higher in newborn PASMC treated with apicidin and HDACi VIII. This was accompanied by increased expression of p21 and reduced expression of CCND1 but not p53. HDAC inhibition altered histone codes around the p21 promoter region in NPASMC. Apicidin inhibited serum-induced cell migration, and modulated profiling of expression of genes encoding pro-oxidant and antioxidant enzymes. Contractility and global DNA methylation levels of newborn PASMCs were also markedly modulated by apicidin.

conclusionOur results demonstrate that class I HDACs are clearly involved in phenotypic alteration of newborn PASMC.

Indexed as

AcetylationAnimalsAntioxidantsCell Cycle CheckpointsCell MovementCell ProliferationCyclin D1Cyclin-Dependent Kinase Inhibitor p21DNA MethylationFamilial Primary Pulmonary HypertensionG1 PhaseHistone Deacetylase InhibitorsHistone DeacetylasesHistonesHumansHypertension, PulmonaryAntioxidantsCyclin D1Cyclin-Dependent Kinase Inhibitor p21Histone Deacetylase InhibitorsHistone DeacetylasesHistonesTumor Suppressor Protein p53

Identifiers

PMID24460719
PMCPMC3904681
OpenAlexW2041765400

What OpenQuestion holds

Textmetadata
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.