Evidence map›Paper›PMID 21402781›Full record

ArticleMolecular and cellular biology2011

Epigenetic regulation of surfactant protein A gene (SP-A) expression in fetal lung reveals a critical role for Suv39h methyltransferases during development and hypoxia.

Houda Benlhabib, Carole R Mendelson

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.5field-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

30 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Role of NRF2 in immune modulator expression in developing lung.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  5. Review
  6. Article
  7. Article
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  10. The etiologic origins for chronic obstructive pulmonary disease.International journal of chronic obstructive pulmonary disease · 2019
    Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Structure, genetics and function of the pulmonary associated surfactant proteins A and D: The extra-pulmonary role of these C type lectins.Annals of anatomy = Anatomischer Anzeiger : official organ of the Anatomische Gesellschaft · 2017
    Review
  16. Article
  17. Article
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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

2 authors at 1 institution in 1 country.

Houda BenlhabibDepartment of Biochemistry, North Texas March of Dimes Birth Defects Center, The University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, TX 75390-9038, USA.
Carole R Mendelson
The University of Texas Southwestern Medical Center · US

Funding

Mechanisms in the Regulation of SP-A Gene Expression - Renewal - 1 - ResubmissionR01HL050022 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI MAHENDROO, MALA S. · 1993 to 2022
$6.6M
NHLBI NIH HHS 5-R01-HL050022NHLBI NIH HHS R01 HL050022
6 · The paper itself

Abstract

SP-A gene expression is developmentally regulated in fetal lung. Cyclic AMP (cAMP) induction of SP-A expression in human fetal lung type II cells is O(2) dependent and is mediated by increased binding of TTF-1/Nkx2.1 and NF-κB to a critical response element (TBE). This is associated with increased acetylation and decreased methylation of H3K9 at the TBE. Using chromatin immunoprecipitation analysis of fetal lung between 15.5 and 19.0 days of gestation, we observed that the developmental induction of SP-A was associated with increased recruitment of TTF-1, NF-κB, PCAF, and CBP, as well as enhanced acetylation and decreased methylation of histone H3K9 at the TBE. Importantly, expression and TBE binding of the H3K9 methyltransferases, Suv39h1 and Suv39h2, was inversely correlated with the developmental upregulation of SP-A. In human fetal lung epithelial cells, Suv39H1 and Suv39H2 mRNA levels declined with cAMP induction of SP-A. Moreover, hypoxia, which inhibits cAMP stimulation of SP-A, markedly increased Suv39h1 and Suv39h2 binding to the TBE. Finally, short hairpin RNA knockdown of Suv39H1 or Suv39H2 in fetal lung epithelial cells repressed H3K9 methylation and greatly enhanced SP-A expression. Collectively, our findings suggest that Suv39H1 and Suv39H2 are key hypoxia-induced methyltransferases; their decline in fetal lung during late gestation is critical for epigenetic changes resulting in the developmental induction of SP-A.

Indexed as

Cell HypoxiaEpigenesis, GeneticAcetylationCell DifferentiationCells, CulturedChromatin ImmunoprecipitationCyclic AMPEpithelial CellsGene Expression Regulation, DevelopmentalGene Knockdown TechniquesHistone-Lysine N-MethyltransferaseHumansLungMethylationMethyltransferasesNF-kappa BCyclic AMPHistone-Lysine N-MethyltransferaseMethyltransferasesNF-kappa BNKX2-1 protein, humanNuclear ProteinsOxygenp300-CBP-Associated Factorp300-CBP Transcription FactorsPulmonary Surfactant-Associated Protein ARepressor ProteinsRNA, MessengerRNA, Small InterferingSUV39H1 protein, humanSUV39H2 protein, humanTFF1 protein, humanThyroid Nuclear Factor 1Transcription FactorsTrefoil Factor-1Tumor Suppressor Proteins

Identifiers

PMID21402781
PMCPMC3133366
OpenAlexW2171326269

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.