Evidence map›Paper›PMID 12897204›Full record

ArticleThe Journal of clinical investigation2003

Hepatic lipase expression in macrophages contributes to atherosclerosis in apoE-deficient and LCAT-transgenic mice.

Zengxuan Nong, Herminia Gonzalez-Navarro, Marcelo Amar, Lita Freeman, Catherine Knapper, Edward B Neufeld, Beverly J Paigen, Robert F Hoyt, Jamila Fruchart-Najib, Silvia Santamarina-Fojo

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

16 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. 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

10 authors at 3 institutions in 2 countries.

Zengxuan NongMolecular Disease Branch, National Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland 20892, USA.
Herminia Gonzalez-Navarro
Marcelo Amar
Lita Freeman
Catherine Knapper
Edward B Neufeld
Beverly J Paigen
Robert F Hoyt
Jamila Fruchart-Najib
Silvia Santamarina-Fojo
National Heart Lung and Blood Institute · USInstitut Pasteur de Lille · FRJackson Laboratory · US

Funding

Use Of Animal Models To Study Lipid Genes That Modulate AtherosclerosisZIAHL002058 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI REMALEY, ALAN THOMAS · 2009 to 2019
$14.3M
Use Of Animal Models To Study Lipid Genes That Modulate AtherosclerosisZ01HL002058 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI REMALEY, ALAN THOMAS · 1996 to 2008
$5.8M
6 · The paper itself

Abstract

Hepatic lipase (HL) has a well-established role in lipoprotein metabolism. However, its role in atherosclerosis is poorly understood. Here we demonstrate that HL deficiency raises the proatherogenic apoB-containing lipoprotein levels in plasma but reduces atherosclerosis in lecithin cholesterol acyltransferase (LCAT) transgenic (Tg) mice, similar to results previously observed with HL-deficient apoE-KO mice. These findings suggest that HL has functions that modify atherogenic risk that are separate from its role in lipoprotein metabolism. We used bone marrow transplantation (BMT) to generate apoE-KO and apoE-KO x HL-KO mice, as well as LCAT-Tg and LCAT-Tg x HL-KO mice, chimeric for macrophage HL gene expression. Using in situ RNA hybridization, we demonstrated localized production of HL by donor macrophages in the artery wall. We found that expression of HL by macrophages enhances early aortic lesion formation in both apoE-KO and LCAT-Tg mice, without changing the plasma lipid profile, lipoprotein lipid composition, or HL and lipoprotein lipase activities. HL does, however, enhance oxidized LDL uptake by peritoneal macrophages. These combined data demonstrate that macrophage-derived HL significantly contributes to early aortic lesion formation in two independent mouse models and identify a novel mechanism, separable from the role of HL in plasma lipoprotein metabolism, by which HL modulates atherogenic risk in vivo.

Indexed as

AnimalsApolipoproteins EArteriosclerosisBone Marrow TransplantationFemaleGene ExpressionLipaseLipidsLipoprotein LipaseMacrophages, PeritonealMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicPhosphatidylcholine-Sterol O-AcyltransferaseRisk FactorsApolipoproteins ELipaseLipidsLipoprotein LipasePhosphatidylcholine-Sterol O-AcyltransferaseRNA, Messenger

Identifiers

PMID12897204
PMCPMC166288
OpenAlexW2042248967

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.