Evidence map›Paper›PMID 7860760›Full record

ArticleThe Journal of clinical investigation1995

Effect of platelet activating factor-acetylhydrolase on the formation and action of minimally oxidized low density lipoprotein.

A D Watson, M Navab, S Y Hama, A Sevanian, S M Prescott, D M Stafforini, T M McIntyre, B N Du, A M Fogelman, J A Berliner

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
13.1field-weighted citation impact, top 1% 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

68 citing papers in PubMed, 401 citations in OpenAlex.

  1. Review
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  8. Article
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  13. Immunological aspects of atherosclerosis.Seminars in immunopathology · 2014
    Review
  14. Article
  15. Article
  16. Article
  17. Lipid oxidation in carriers of lecithin:cholesterol acyltransferase gene mutations.Arteriosclerosis, thrombosis, and vascular biology · 2012
    Article
  18. Review
  19. Review
  20. Review

8 more citing papers are in PubMed but not listed here.

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

10 authors at 1 institution in 1 country.

A D WatsonDepartment of Pathology, University of California, Los Angeles 90024.
M Navab
S Y Hama
A Sevanian
S M Prescott
D M Stafforini
T M McIntyre
B N Du
A M Fogelman
J A Berliner
University of California, Los Angeles · US

Funding

ULTRASTRUCTURE OF THE INTIMA IN EARLY LESION FORMATIONP01HL030568 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI FOGELMAN, ALAN M · 1985 to 2019
$55.2M
ENDOTHELIAL PHOSPHOLIPASE A2 IN OXIDANT MEMBRANE INJURYR01HL045206 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI SEVANIAN, ALEX · 1991 to 1997
–
NHLBI NIH HHS HL-07386NHLBI NIH HHS HL-30568NHLBI NIH HHS HL-45206
6 · The paper itself

Abstract

Mildly oxidized low density lipoprotein (MM-LDL) produced by oxidative enzymes or cocultures of human artery wall cells induces endothelial cells to produce monocyte chemotactic protein-1 and to bind monocytes. HDL prevents the formation of MM-LDL by cocultures of artery wall cells. Using albumin treatment and HPLC we have isolated and partially characterized bioactive oxidized phospholipids in MM-LDL. Platelet activating factor-acetylhydrolase (PAF-AH), a serine esterase, hydrolyzes short chain acyl groups esterified to the sn-2 position of phospholipids such as PAF and particular oxidatively fragmented phospholipids. Treatment of MM-LDL with PAF-AH (2-4 x 10(-2) U/ml) eliminated the ability of MM-LDL to induce endothelial cells to bind monocytes. When HDL protected against the formation of MM-LDL by cocultures, lysophosphatidylcholine was detected in HDL; whereas when HDL was pretreated with diisopropyl fluorophosphate, HDL was no longer protective and lysophosphatidylcholine was undetectable. HPLC analysis also revealed that the active oxidized phospholipid species in MM-LDL had been destroyed after PAF-AH treatment. In addition, treatment of MM-LDL with albumin removed polar phospholipids that, when reisolated, induced monocyte binding to endothelial cells. These polar phospholipids, when treated with PAF-AH, lost biological activity and were no longer detected by HPLC. These results suggest that PAF-AH in HDL protects against the production and activity of MM-LDL by facilitating hydrolysis of active oxidized phospholipids to lysolipids, thereby destroying the biologically active lipids in MM-LDL.

Indexed as

1-Alkyl-2-acetylglycerophosphocholine EsteraseAnimalsAortaCell AdhesionCell CommunicationCell MovementCells, CulturedChromatography, High Pressure LiquidChromatography, Thin LayerEndothelium, VascularHumansLipoproteins, HDLLipoproteins, LDLMonocytesMuscle, Smooth, VascularPhospholipases A1-Alkyl-2-acetylglycerophosphocholine EsteraseLipoproteins, HDLLipoproteins, LDLPhospholipases APhospholipidsSerum Albumin

Identifiers

PMID7860760
PMCPMC295551
OpenAlexW2080486016

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.