Evidence map›Paper›PMID 20498409›Full record

ArticleJournal of lipid research2010

Genetic deletion of apolipoprotein A-I increases airway hyperresponsiveness, inflammation, and collagen deposition in the lung.

Weiling Wang, Hao Xu, Yang Shi, Sandhya Nandedkar, Hao Zhang, Haiqing Gao, Thom Feroah, Dorothee Weihrauch, Marie L Schulte, Deron W Jones and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

51 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Cholesterol Accumulation Enhances Cigarette Smoke-Induced Airway Epithelial Inflammation.International journal of chronic obstructive pulmonary disease · 2025
    Article
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  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Rat bronchoalveolar lavage proteome changes following e-cigarette aerosol exposures.American journal of physiology. Lung cellular and molecular physiology · 2023
    Article
  13. High-Density Lipoproteins: A Role in Inflammation in COPD.International journal of molecular sciences · 2022
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  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

13 authors at 4 institutions in 2 countries.

Weiling WangDepartment of Surgery, Medical College of Wisconsin, Milwaukee, WI, USA.
Hao Xu
Yang Shi
Sandhya Nandedkar
Hao Zhang
Haiqing Gao
Thom Feroah
Dorothee Weihrauch
Marie L Schulte
Deron W Jones
Jason Jarzembowski
Mary Sorci-Thomas
Kirkwood A Pritchard
Medical College of Wisconsin · USChildren's Hospital of Wisconsin · USShandong University · CNWake Forest University · US

Funding

TISSUE CULTURE COREP01HL049373 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI SHELNESS, GREGORY S · 1993 to 2012
$23.8M
Asthma and Nocturnal Hypoxemia in Sickle Cell Anemia IIR01HL079937 · NHLBI · WASHINGTON UNIVERSITY · PI DEBAUN, MICHAEL R., STRUNK, ROBERT · 2005 to 2013
$10.4M
Inflammation, Atherosclerosis and ApoA-IR01HL064163 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI SORCI-THOMAS, MARY G · 2000 to 2013
$4.1M
T Regulatory Lymphocytes, HDL Function, and AtherosclerosisR01HL112276 · NHLBI · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI HEDRICK, CATHERINE C, SORCI-THOMAS, MARY G · 2013 to 2016
$2.8M
Biophysics of HDL DysfunctionR01HL112270 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI PRITCHARD, KIRKWOOD ARTHUR, SORCI-THOMAS, MARY G · 2012 to 2015
$2.5M
Inflammation, fibrosis and myocardial function in schlerodermaR01HL089779 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI WEIHRAUCH, DOROTHEE · 2008 to 2012
$2.2M
Biogenesis of HDL Through Cholesterol Efflux and ApoA-I Structural ReorganizationR01HL127649 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI SORCI-THOMAS, MARY G · 2015 to 2018
$2.2M
HDL Dysfunction and Vascular InflammationR01HL081139 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI PRITCHARD, KIRKWOOD ARTHUR · 2006 to 2010
$1.8M
NHLBI NIH HHS HL-079937NHLBI NIH HHS HL-081139NHLBI NIH HHS HL-089779NHLBI NIH HHS HL-49373NHLBI NIH HHS HL-64163NHLBI NIH HHS P01 HL049373NHLBI NIH HHS R01 HL064163NHLBI NIH HHS R01 HL079937NHLBI NIH HHS R01 HL081139NHLBI NIH HHS R01 HL089779NHLBI NIH HHS R01 HL112270NHLBI NIH HHS R01 HL112276NHLBI NIH HHS R01 HL127649
6 · The paper itself

Abstract

The relationship between high-density lipoprotein and pulmonary function is unclear. To determine mechanistic relationships we investigated the effects of genetic deletion of apolipoprotein A-I (apoA-I) on plasma lipids, paraoxonase (PON1), pro-inflammatory HDL (p-HDL), vasodilatation, airway hyperresponsiveness and pulmonary oxidative stress, and inflammation. ApoA-I null (apoA-I(-/-)) mice had reduced total and HDL cholesterol but increased pro-inflammatory HDL compared with C57BL/6J mice. Although PON1 protein was increased in apoA-I(-/-) mice, PON1 activity was decreased. ApoA-I deficiency did not alter vasodilatation of facialis arteries, but it did alter relaxation responses of pulmonary arteries. Central airway resistance was unaltered. However, airway resistance mediated by tissue dampening and elastance were increased in apoA-I(-/-) mice, a finding also confirmed by positive end-expiratory pressure (PEEP) studies. Inflammatory cells, collagen deposition, 3-nitrotyrosine, and 4-hydroxy-2-nonenal were increased in apoA-I(-/-) lungs but not oxidized phospholipids. Colocalization of 4-hydroxy-2-nonenal with transforming growth factor beta-1 (TGFbeta-1 was increased in apoA-I(-/-) lungs. Xanthine oxidase, myeloperoxidase and endothelial nitric oxide synthase were increased in apoA-I(-/-) lungs. Dichlorodihydrofluorescein-detectable oxidants were increased in bronchoalveolar lavage fluid (BALF) in apoA-I(-/-) mice. In contrast, BALF nitrite+nitrate levels were decreased in apoA-I(-/-) mice. These data demonstrate that apoA-I plays important roles in limiting pulmonary inflammation and oxidative stress, which if not prevented, will decrease pulmonary artery vasodilatation and increase airway hyperresponsiveness.

Indexed as

LungAnimalsApolipoprotein A-IAryldialkylphosphataseBiomarkersBronchial HyperreactivityBronchoalveolar Lavage FluidCholesterol, HDLCollagenGene DeletionInflammationLipid MetabolismMaleMiceMice, Inbred C57BLOxidative StressApolipoprotein A-IAryldialkylphosphataseBiomarkersCholesterol, HDLCollagen

Identifiers

PMID20498409
PMCPMC2918439
OpenAlexW2039551737

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.