Evidence map›Paper›PMID 19130898›Full record

ArticleBiochimica et biophysica acta2009

Expression of phospholipases A2 in primary human lung macrophages: role of cytosolic phospholipase A2-alpha in arachidonic acid release and platelet activating factor synthesis.

Giorgio Giannattasio, Ying Lai, Francescopaolo Granata, Carine M Mounier, Laxman Nallan, Rob Oslund, Christina C Leslie, Gianni Marone, Gérard Lambeau, Michael H Gelb and 1 more

Open access · greenAbstract read
In one paragraph

Article in Biochimica et biophysica acta, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.0field-weighted citation impact, top 27% 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

15 citing papers in PubMed, 29 citations in OpenAlex.

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  15. Lung mast cells are a source of secreted phospholipases A2.The Journal of allergy and clinical immunology · 2009
    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

11 authors at 7 institutions in 3 countries.

Giorgio GiannattasioDepartment of Clinical Immunology and Allergy and Center for Basic and Clinical Immunology Research (CISI), University of Naples Federico II, Via S. Pansini 5, 80131 Naples, Italy.
Ying Lai
Francescopaolo Granata
Carine M Mounier
Laxman Nallan
Rob Oslund
Christina C Leslie
Gianni Marone
Gérard Lambeau
Michael H Gelb
Massimo Triggiani
University of Naples Federico II · ITSeattle University · USCentre National de la Recherche Scientifique · FRInstitut de Pharmacologie Moléculaire et Cellulaire · FRUniversity of Colorado Denver · USUniversity of Washington · USUniversity of Washington Applied Physics Laboratory · US

Funding

TRANSLOCATION AND TRANSCELLULAR BIOSYNTHESISP01HL034303 · NHLBI · NATIONAL JEWISH HEALTH · PI BARKLEY, ROBERT · 1985 to 2015
$25.0M
Biochemical Studies of 14-kDa Phospholipases A2R37HL036235 · NHLBI · UNIVERSITY OF WASHINGTON · PI GELB, MICHAEL H · 2007 to 2016
$4.1M
Regulation and Function of Cytosolic Phospholipase A2R01HL050040 · NHLBI · UNIVERSITY OF WASHINGTON · PI GELB, MICHAEL H · 1993 to 2012
$2.4M
STUDIES IN ENZYMOLOGY USING INHIBITORSR01HL036235 · NHLBI · UNIVERSITY OF WASHINGTON · PI GELB, MICHAEL H · 1989 to 2006
$2.1M
RATIONALLY-DESIGNED INHIBITORS OF PHOSPHOLIPASE-A2R23HL036235 · NHLBI · UNIVERSITY OF WASHINGTON · PI GELB, MICHAEL H · 1986 to 1988
–
NHLBI NIH HHS HL34303NHLBI NIH HHS HL36235NHLBI NIH HHS HL50040NHLBI NIH HHS P01 HL034303NHLBI NIH HHS R01 HL036235NHLBI NIH HHS R01 HL050040NHLBI NIH HHS R37 HL036235
6 · The paper itself

Abstract

Macrophages are a major source of lipid mediators in the human lung. Expression and contribution of cytosolic (cPLA(2)) and secreted phospholipases A(2) (sPLA(2)) to the generation of lipid mediators in human macrophages are unclear. We investigated the expression and role of different PLA(2)s in the production of lipid mediators in primary human lung macrophages. Macrophages express the alpha, but not the zeta isoform of group IV and group VIA cPLA(2) (iPLA(2)). Two structurally-divergent inhibitors of group IV cPLA(2) completely block arachidonic acid release by macrophages in response to non-physiological (Ca(2+) ionophores and phorbol esters) and physiological agonists (lipopolysaccharide and Mycobacterium protein derivative). These inhibitors also reduce by 70% the synthesis of platelet-activating factor by activated macrophages. Among the full set of human sPLA(2)s, macrophages express group IIA, IID, IIE, IIF, V, X and XIIA, but not group IB and III enzymes. Me-Indoxam, a potent and cell impermeable inhibitor of several sPLA(2)s, has no effect on arachidonate release or platelet-activating factor production. Agonist-induced exocytosis is not influenced by cPLA(2) inhibitors at concentrations that block arachidonic acid release. Our results indicate that human macrophages express cPLA(2)-alpha, iPLA(2) and several sPLA(2)s. Cytosolic PLA(2)-alpha is the major enzyme responsible for lipid mediator production in human macrophages.

Indexed as

Arachidonic AcidCarbamatesCells, CulturedEnzyme InhibitorsExocytosisFluoroimmunoassayGlucuronidaseGroup IV Phospholipases A2HumansImmunoblottingIndolizinesIonophoresLipopolysaccharidesMacrophages, AlveolarPlatelet Activating FactorPolymerase Chain ReactionArachidonic AcidCarbamatesEnzyme InhibitorsGlucuronidaseGroup IV Phospholipases A2IndolizinesindoxamIonophoresLipopolysaccharidesPlatelet Activating Factor

Identifiers

PMID19130898
PMCPMC2676353
OpenAlexW1590776570

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.