Evidence map›Paper›PMID 1401083›Full record

ArticleThe Journal of clinical investigation1992

Lipoprotein lipase-mediated uptake and degradation of low density lipoproteins by fibroblasts and macrophages.

S C Rumsey, J C Obunike, Y Arad, R J Deckelbaum, I J Goldberg

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
12.2field-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

32 citing papers in PubMed, 192 citations in OpenAlex.

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  7. Control of organization and function of muscle and tendon by thrombospondin-4.Matrix biology : journal of the International Society for Matrix Biology · 2014
    Article
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  10. Review
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  12. n-3, but not n-6 lipid particle uptake requires cell surface anchoring.Biochemical and biophysical research communications · 2010
    Article
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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

5 authors at 1 institution in 1 country.

S C RumseyDepartment of Pediatrics, Columbia University College of Physicians and Surgeons, New York 10032.
J C Obunike
Y Arad
R J Deckelbaum
I J Goldberg
Columbia University · US

Funding

Pathways of Tissue Lipid UptakeR01HL045095 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ABUMRAD, NADA A., GOLDBERG, IRA J · 1991 to 2024
$6.9M
EXTRACELLULAR REGULATION OF LIPOPROTEIN LIPASE ACTIVITYR37HL045095 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GOLDBERG, IRA J · 2000 to 2009
$4.6M
METABOLISM OF INTRAVENOUS LIPID EMULSIONSR01HL040404 · NHLBI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI DECKELBAUM, RICHARD JOSEPH · 1988 to 2008
$2.9M
VITAMIN A TRANSPORT AND RETINOL-BINDING PROTEIN METABOLISMP50HL021006 · NHLBI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI TALL, ALAN RICHARD · 1985 to 1996
–
NHLBI NIH HHS HL-21006NHLBI NIH HHS HL-40404NHLBI NIH HHS HL-45095
6 · The paper itself

Abstract

Lipoprotein lipase (LPL), the rate limiting enzyme for hydrolysis of lipoprotein triglyceride, also mediates nonenzymatic interactions between lipoproteins and heparan sulfate proteoglycans. To determine whether cell surface LPL increases LDL binding to cells, bovine milk LPL was added to upregulated and nonupregulated human fibroblasts along with media containing LDL. LDL binding to cells was increased 2-10-fold, in a dose-dependent manner, by the addition of 0.5-10 micrograms/ml of LPL. The amount of LDL bound to the cells in the presence of LPL far exceeded the capacity for LDL binding via the LDL receptor. Treatment of fibroblasts with heparinase and heparitinase resulted in a 64% decrease in LPL-mediated LDL binding. Compared to studies performed without LPL, more LDL was internalized and degraded in the presence of LPL, but the time course was slower than that of classical lipoprotein receptor mediated pathways. In LDL receptor negative fibroblasts, LPL increased surface bound LDL > 140-fold, intracellular LDL > 40-fold, and LDL degradation > 6-fold. These effects were almost completely inhibited by heparin and anti-LPL monoclonal antibody. LPL also increased the binding and uptake by fibroblasts of apolipoprotein-free triglyceride emulsions; binding was increased > 8-fold and cellular uptake was increased > 40-fold with LPL. LPL increased LDL binding to THP-1 monocytes, and increased LDL uptake (4.5-fold) and LDL degradation (2.5-fold) by THP-1 macrophages. In the absence of added LPL, heparin and anti-LPL monoclonal antibodies decreased LDL degradation by > 40%, and triglyceride emulsion uptake by > 50%, suggesting that endogenously produced LPL mediated lipid particle uptake and degradation. We conclude that LPL increases lipid and lipoprotein uptake by cells via a pathway not involving the LDL receptor. This pathway may be important for lipid accumulation in LPL synthesizing cells.

Indexed as

AnimalsCattleCells, CulturedEmulsionsFibroblastsHeparin LyaseHumansLipoprotein LipaseLipoproteins, LDLMacrophagesPolysaccharide-LyasesReceptors, LDLTriglyceridesEmulsionsHeparin LyaseLipoprotein LipaseLipoproteins, LDLPolysaccharide-LyasesReceptors, LDLTriglycerides

Identifiers

PMID1401083
PMCPMC443197
OpenAlexW2155759352

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.