Evidence map›Paper›PMID 21821728›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2011

Lysophosphatidic acid receptor 1 modulates lipopolysaccharide-induced inflammation in alveolar epithelial cells and murine lungs.

Jing Zhao, Donghong He, Yanlin Su, Evgeny Berdyshev, Jerold Chun, Viswanathan Natarajan, Yutong Zhao

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.5field-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

43 citing papers in PubMed, 68 citations in OpenAlex.

  1. Lysophosphatidic Acid Receptor 5 (LPAInternational journal of molecular sciences · 2026
    Article
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  6. Lysophosphatidic acid receptor 1 inhibition: a potential treatment target for pulmonary fibrosis.European respiratory review : an official journal of the European Respiratory Society · 2024
    Review
  7. Autotaxin Has a Negative Role in Systemic Inflammation.International journal of molecular sciences · 2022
    Article
  8. Article
  9. Article
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  11. Article
  12. Review
  13. Article
  14. Review
  15. Lysophospholipids in Lung Inflammatory Diseases.Advances in experimental medicine and biology · 2021
    Article
  16. Article
  17. Review
  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

7 authors at 3 institutions in 1 country.

Jing ZhaoDepartment of Medicine, University of Pittsburgh School of Medicine, PA 15213, USA.
Donghong He
Yanlin Su
Evgeny Berdyshev
Jerold Chun
Viswanathan Natarajan
Yutong Zhao
University of Illinois Chicago · USUniversity of Pittsburgh · USScripps Research Institute · US

Funding

Lysophosphatidic Acid in Airway Barrier Function and RemodelingR01HL091916 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ZHAO, YUTONG · 2009 to 2013
$1.8M
Protective Role of Intracellular S1P in Lung InjuryR37HL079396 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI NATARAJAN, VISWANATHAN · 2010 to 2010
$393k
NHLBI NIH HHS HL-0911916NHLBI NIH HHS HL-R37 079396NHLBI NIH HHS R01 HL091916
6 · The paper itself

Abstract

Lysophosphatidic acid (LPA), a bioactive phospholipid, plays an important role in lung inflammation by inducing the release of chemokines and lipid mediators. Our previous studies have shown that LPA induces the secretion of interleukin-8 and prostaglandin E(2) in lung epithelial cells. Here, we demonstrate that LPA receptors contribute to lipopolysaccharide (LPS)-induced inflammation. Pretreatment with LPA receptor antagonist Ki16425 or downregulation of LPA receptor 1 (LPA(1)) by small-interfering RNA (siRNA) attenuated LPS-induced phosphorylation of p38 MAPK, I-κB kinase, and I-κB in MLE12 epithelial cells. In addition, the blocking of LPA(1) also suppressed LPS-induced IL-6 production. Furthermore, LPS treatment promoted interaction between LPA(1) and CD14, a LPS coreceptor, in a time- and dose-dependent manner. Disruption of lipid rafts attenuated the interaction between LPA(1) and CD14. Mice challenged with LPS increased plasma LPA levels and enhanced expression of LPA receptors in lung tissues. To further investigate the role of LPA receptors in LPS-induced inflammation, wild-type, or LPA(1)-deficient mice, or wild-type mice pretreated with Ki16425 were intratracheally challenged with LPS for 24 h. Knock down or inhibition of LPA(1) decreased LPS-induced IL-6 release in bronchoalveolar lavage (BAL) fluids and infiltration of cells into alveolar space compared with wild-type mice. However, no significant differences in total protein concentration in BAL fluids were observed. These results showed that knock down or inhibition of LPA(1) offered significant protection against LPS-induced lung inflammation but not against pulmonary leak as observed in the murine model for lung injury.

Indexed as

Receptors, Lysophosphatidic AcidAnimalsBronchiBronchoalveolar Lavage FluidCells, CulturedEpithelial CellsGene Expression RegulationInflammationInterleukin-6Interleukin-8IsoxazolesLipopolysaccharide ReceptorsLipopolysaccharidesLysophospholipidsMaleMembrane Microdomains3-(4-(4-((1-(2-chlorophenyl)ethoxy)carbonyl amino)-3-methyl-5-isoxazolyl) benzylsulfanyl) propanoic acidInterleukin-6Interleukin-8IsoxazolesLipopolysaccharide ReceptorsLipopolysaccharideslysophosphatidic acidLysophospholipidsNF-kappa Bp38 Mitogen-Activated Protein KinasesPropionatesReceptors, Lysophosphatidic Acid

Identifiers

PMID21821728
PMCPMC3191756
OpenAlexW2061205998

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.