Evidence map›Paper›PMID 24671012›Full record

ArticleJournal of lipid research2014

The macrophage LBP gene is an LXR target that promotes macrophage survival and atherosclerosis.

Tamer Sallam, Ayaka Ito, Xin Rong, Jason Kim, Caroline van Stijn, Brian T Chamberlain, Michael E Jung, Lily C Chao, Marius Jones, Thomas Gilliland and 5 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of lipid research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

18 citing papers in PubMed, 30 citations in OpenAlex.

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  10. Immune Biomarkers in the Prediction of Future Myocardial Infarctions in People With Human Immunodeficiency Virus.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2020
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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

15 authors at 4 institutions in 1 country.

Tamer SallamDivision of Cardiology, Department of Medicine, University of California, Los Angeles, Los Angeles, CA Howard Hughes Medical Institute, University of California, Los Angeles, Los Angeles, CA.
Ayaka ItoDepartment of Pathology and Laboratory Medicine, University of California, Los Angeles, Los Angeles, CA Howard Hughes Medical Institute, University of California, Los Angeles, Los Angeles, CA.
Xin RongDepartment of Pathology and Laboratory Medicine, University of California, Los Angeles, Los Angeles, CA Howard Hughes Medical Institute, University of California, Los Angeles, Los Angeles, CA.
Jason KimDepartment of Medicine, Division of Endocrinology, University of California, Los Angeles, Los Angeles, CA.
Caroline van StijnDepartment of Medicine, Division of Endocrinology, University of California, Los Angeles, Los Angeles, CA.
Brian T ChamberlainDepartment of Chemistry and Biochemistry, California NanoSystems Institute, University of California, Los Angeles, Los Angeles, CA.
Michael E JungDepartment of Chemistry and Biochemistry, California NanoSystems Institute, University of California, Los Angeles, Los Angeles, CA.
Lily C ChaoSaban Research Institute, Children's Hospital Los Angeles, University of Southern California, Los Angeles, CA.
Marius JonesDepartment of Pathology and Laboratory Medicine, University of California, Los Angeles, Los Angeles, CA Howard Hughes Medical Institute, University of California, Los Angeles, Los Angeles, CA.
Thomas GillilandDepartment of Pathology and Laboratory Medicine, University of California, Los Angeles, Los Angeles, CA Howard Hughes Medical Institute, University of California, Los Angeles, Los Angeles, CA.
XiaoHui WuDivision of Cardiology, Department of Medicine, University of California, Los Angeles, Los Angeles, CA.
Grace L SuMedical Service, Department of Veterans Affairs Medical Center, Ann Arbor, MI Department of Medicine, University of Michigan Medical School, Ann Arbor, MI.
Rajendra K TangiralaDepartment of Medicine, Division of Endocrinology, University of California, Los Angeles, Los Angeles, CA.
Peter TontonozDepartment of Pathology and Laboratory Medicine, University of California, Los Angeles, Los Angeles, CA Howard Hughes Medical Institute, University of California, Los Angeles, Los Angeles, CA.
Cynthia HongDepartment of Pathology and Laboratory Medicine, University of California, Los Angeles, Los Angeles, CA Howard Hughes Medical Institute, University of California, Los Angeles, Los Angeles, CA.
University of California, Los Angeles · USHoward Hughes Medical Institute · USUniversity of Michigan · USUniversity of Southern California · US

Funding

Transgenic & Knock-out MouseP30DK063491 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI PETER J TONTONOZ · 2003 to 2026
$40.4M
Pilot and Feasibility ProgramP30DK041301 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 1990 to 2019
$18.0M
CARDIOVASCULAR SCIENTIST TRAINING PROGRAMT32HL007895 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SHIVKUMAR, KALYANAM, WATSON, KAROL E · 1998 to 2023
$9.2M
Adiponectin Actions on the Monocyte to Reduce AtherosclerosisR01HL086566 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TANGIRALA, RAJENDRA K · 2009 to 2013
$1.9M
NHLBI NIH HHS R01 HL086566NHLBI NIH HHS T32 HL007895NIDDK NIH HHS P30 DK041301NIDDK NIH HHS P30 DK063491
6 · The paper itself

Abstract

The liver X receptors (LXRs) are members of the nuclear receptor superfamily that regulate sterol metabolism and inflammation. We sought to identify previously unknown genes regulated by LXRs in macrophages and to determine their contribution to atherogenesis. Here we characterize a novel LXR target gene, the lipopolysaccharide binding protein (LBP) gene. Surprisingly, the ability of LXRs to control LBP expression is cell-type specific, occurring in macrophages but not liver. Treatment of macrophages with oxysterols or loading with modified LDL induces LBP in an LXR-dependent manner, suggesting a potential role for LBP in the cellular response to cholesterol overload. To investigate this further, we performed bone marrow transplant studies. After 18 weeks of Western diet feeding, atherosclerotic lesion burden was assessed revealing markedly smaller lesions in the LBP(-/-) recipients. Furthermore, loss of bone marrow LBP expression increased apoptosis in atherosclerotic lesions as determined by terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Supporting in vitro studies with isolated macrophages showed that LBP expression does not affect cholesterol efflux but promotes the survival of macrophages in the setting of cholesterol loading. The LBP gene is a macrophage-specific LXR target that promotes foam cell survival and atherogenesis.

Indexed as

ApoptosisAcute-Phase ProteinsAnimalsAtherosclerosisCarrier ProteinsCell SurvivalFoam CellsLipopolysaccharide-Binding ProteinLipoproteins, LDLLiver X ReceptorsMembrane GlycoproteinsMiceMice, KnockoutAcute-Phase ProteinsCarrier ProteinsLipopolysaccharide-Binding ProteinLipoproteins, LDLLiver X ReceptorsMembrane Glycoproteinsatherogenesislipopolysaccharide binding proteinliver X receptornuclear receptor

Identifiers

PMID24671012
PMCPMC4031943
OpenAlexW1995892391

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.