Evidence map›Paper›PMID 18566389›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2008

Peroxisome proliferator-activated receptor-gamma regulates the expression of alveolar macrophage macrophage colony-stimulating factor.

Tracey L Bonfield, Mary Jane Thomassen, Carol F Farver, Susamma Abraham, Mary T Koloze, Xia Zhang, David M Mosser, Daniel A Culver

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

32 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Enhancing Cystic Fibrosis Immune Regulation.Frontiers in pharmacology · 2021
    Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Mesenchymal Stem Cell Soluble Mediators and Cystic Fibrosis.Journal of stem cell research & therapy · 2017
    Article
  13. Article
  14. Article
  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

8 authors at 4 institutions in 1 country.

Tracey L BonfieldDepartment of Pediatrics, Case Western Reserve University, Cleveland, OH 44109, USA. tracey.bonfield@case.edu
Mary Jane Thomassen
Carol F Farver
Susamma Abraham
Mary T Koloze
Xia Zhang
David M Mosser
Daniel A Culver
Cleveland Clinic · USUniversity of Maryland, College Park · USCase Western Reserve University · USEast Carolina University · US

Funding

MODULATING HOST RESPONSES TO BACTERIAL PRODUCTSR01AI049383 · NIAID · UNIV OF MARYLAND, COLLEGE PARK · PI MOSSER, DAVID M · 2001 to 2011
$3.1M
NIAID NIH HHS R01 AI049383
6 · The paper itself

Abstract

Macrophage CSF (M-CSF) regulates monocyte differentiation, activation, and foam cell formation. We have observed that it is elevated in human pulmonary alveolar proteinosis (PAP) and in the GM-CSF knockout mouse, a murine model for PAP. A potential regulator of M-CSF, peroxisome proliferator-activated receptor-gamma (PPARgamma), is severely deficient in both human PAP and the GM-CSF knockout mouse. To investigate the role of PPARgamma in alveolar macrophage homeostasis, we generated myeloid-specific PPARgamma knockout mice using the Lys-Cre method to knock out the floxed PPARgamma gene. Similar to the GM-CSF-deficient mouse, absence of alveolar macrophage PPARgamma resulted in development of lung pathology resembling PAP in 16-wk-old mice, along with excess M-CSF gene expression and secretion. In ex vivo wild-type alveolar macrophages, we observed that M-CSF itself is capable of inducing foam cell formation similar to that seen in PAP. Overexpression of PPARgamma prevented LPS-stimulated M-CSF production in RAW 264.7 cells, an effect that was abrogated by a specific PPARgamma antagonist, GW9662. Use of proteasome inhibitor, MG-132 or a PPARgamma agonist, pioglitazone, prevented LPS-mediated M-CSF induction. Using chromatin immunoprecipitation, we found that PPARgamma is capable of regulating M-CSF through transrepression of NF-kappaB binding at the promoter. Gel-shift assay experiments confirmed that pioglitazone is capable of blocking NF-kappaB binding. Taken together, these data suggest that M-CSF is an important mediator of alveolar macrophage homeostasis, and that transcriptional control of M-CSF production is regulated by NF-kappaB and PPARgamma.

Indexed as

AnimalsCells, CulturedGene Expression RegulationHumansMacrophage Colony-Stimulating FactorMacrophages, AlveolarMiceMice, KnockoutNF-kappa BPhenotypePioglitazonePPAR gammaPromoter Regions, GeneticProtein BindingResponse ElementsThiazolidinedionesMacrophage Colony-Stimulating FactorNF-kappa BPioglitazonePPAR gammaThiazolidinediones

Identifiers

PMID18566389
PMCPMC2819287
OpenAlexW2167634177

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.