Evidence map›Paper›PMID 16127159›Full record

ArticleThe American journal of pathology2005

Neutral lipids and peroxisome proliferator-activated receptor-{gamma} control pulmonary gene expression and inflammation-triggered pathogenesis in lysosomal acid lipase knockout mice.

Xuemei Lian, Cong Yan, Yulin Qin, Lana Knox, Tingyu Li, Hong Du

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

39 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Lysosomal Acid Lipase in Lipid Metabolism and Beyond.Arteriosclerosis, thrombosis, and vascular biology · 2019
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Atherogenic high cholesterol/high fat diet induces TLRs-associated pulmonary inflammation in C57BL/6J mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Epigenetic contributions to the developmental origins of adult lung disease.Biochemistry and cell biology = Biochimie et biologie cellulaire · 2015
    Review
  19. Article
  20. 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

6 authors at 2 institutions in 2 countries.

Xuemei LianDivision of Pulmonary Biology, or Hong Du, Ph.D., Division of Human Genetics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229-3039, USA.
Cong Yan
Yulin Qin
Lana Knox
Tingyu Li
Hong Du
Cincinnati Children's Hospital Medical Center · USChongqing Medical University · CN

Funding

RETINOIC ACID RECEPTOR AND SP-B GENE REGULATIONR01HL061803 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI YAN, CONG · 1999 to 2006
$1.9M
Nuclear Receptor Co-Activators in the LungR01HL067862 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI YAN, CONG · 2003 to 2006
$1.5M
NHLBI NIH HHS HL-061803NHLBI NIH HHS HL-067862NHLBI NIH HHS R01 HL061803NHLBI NIH HHS R01 HL067862
6 · The paper itself

Abstract

The functional roles of neutral lipids in the lung are poorly understood. However, blocking cholesteryl ester and triglyceride metabolism in lysosomal acid lipase gene knockout mice (lal-/-) results in severe pathogenic phenotypes in the lung, including massive neutrophil infiltration, foamy macrophage accumulation, unwanted cell growth, and emphysema. To elucidate the mechanism underlining these pathologies, we performed Affymetrix GeneChip microarray analysis of 1-, 3-, and 6-month-old mice and identified aberrant gene expression that progressed with age. Among changed genes, matrix metalloproteinase (MMP)-12, apoptosis inhibitor 6 (Api-6), erythroblast transformation-specific domain (Ets) transcription factor family member Spi-C, and oncogene MafB were increased 100-, 70-, 40-, and 10-fold, respectively, in lal-/- lungs versus the wild-type lungs. The pathogenic increases of these molecules occurred primarily in alveolar type II epithelial cells. Transcriptional activities of the MMP-12 and Api-6 promoters were stimulated by Spi-C or MafB in respiratory epithelial cells. Treatment with 9-hydroxyoctadecanoic acids and ciglitazone significantly rescued lal-/- pulmonary inflammation and aberrant gene expression. In addition, both compounds as well as peroxisome proliferator-activated receptor gamma inhibited MMP-12 and Api-6 promoter activities. These data suggest that inflammation-triggered cell growth and emphysema during lysosomal acid lipase deficiency are partially caused by peroxisome proliferator-activated receptor-gamma inactivation.

Indexed as

Gene Expression RegulationLipid MetabolismAnimalsApoptosis Regulatory ProteinsBronchoalveolar Lavage FluidDNA-Binding ProteinsGene Expression ProfilingInflammationLungLung DiseasesMafB Transcription FactorMatrix Metalloproteinase 12MetalloendopeptidasesMiceMice, KnockoutOligonucleotide Array Sequence AnalysisApoptosis Regulatory ProteinsCd5l protein, mouseDNA-Binding Proteinslysosomal acid lipase, mouseMafb protein, mouseMafB Transcription FactorMatrix Metalloproteinase 12MetalloendopeptidasesOncogene ProteinsPPAR gammaReceptors, ImmunologicReceptors, ScavengerSpic protein, mouseSterol EsteraseTranscription Factors

Identifiers

PMID16127159
PMCPMC1698726
OpenAlexW2014827601

What OpenQuestion holds

Textmetadata
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.