Evidence map›Paper›PMID 24489659›Full record

ArticlePloS one2014

Deficiency of CCAAT/enhancer binding protein-epsilon reduces atherosclerotic lesions in LDLR-/- mice.

Ryoko Okamoto, Sigal Gery, Adrian F Gombart, Xuping Wang, Lawrence W Castellani, Tadayuki Akagi, Shuang Chen, Moshe Arditi, Quoc Ho, Aldons J Lusis and 2 more

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

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.1field-weighted citation impact, top 46% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. 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

12 authors at 2 institutions in 2 countries.

Ryoko OkamotoDivision of Hematology and Oncology, Cedars-Sinai Medical Center, University of California Los Angeles (UCLA) School of Medicine, Los Angeles, California, United States of America.
Sigal GeryDivision of Hematology and Oncology, Cedars-Sinai Medical Center, University of California Los Angeles (UCLA) School of Medicine, Los Angeles, California, United States of America.
Adrian F GombartDivision of Hematology and Oncology, Cedars-Sinai Medical Center, University of California Los Angeles (UCLA) School of Medicine, Los Angeles, California, United States of America ; Department of Biochemisty and Biophysics, Linus Pauling Institute, Oregon State University, Corvallis, Oregon, United States of America.
Xuping WangDepartment of Human Genetics, Department of Medicine, and Department of Microbiology, Molecular Genetics, and Immunology, David Geffen School of Medicine at University of California Los Angeles (UCLA), Los Angeles, California, United States of America.
Lawrence W CastellaniDepartment of Medicine/Division of Cardiology, David Geffen School of Medicine at University of California Los Angeles (UCLA), Los Angeles, California, United States of America.
Tadayuki AkagiDivision of Hematology and Oncology, Cedars-Sinai Medical Center, University of California Los Angeles (UCLA) School of Medicine, Los Angeles, California, United States of America.
Shuang ChenDivision of Pediatric Infectious Diseases and Immunology, Cedars-Sinai Medical Center, Los Angeles, California, United States of America.
Moshe ArditiDivision of Pediatric Infectious Diseases and Immunology, Cedars-Sinai Medical Center, Los Angeles, California, United States of America.
Quoc HoDivision of Hematology and Oncology, Cedars-Sinai Medical Center, University of California Los Angeles (UCLA) School of Medicine, Los Angeles, California, United States of America.
Aldons J LusisDepartment of Human Genetics, Department of Medicine, and Department of Microbiology, Molecular Genetics, and Immunology, David Geffen School of Medicine at University of California Los Angeles (UCLA), Los Angeles, California, United States of America.
Quanlin LiBiostatistics and Bioinformatics Research Center, Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, California, United States of America.
H Phillip KoefflerDivision of Hematology and Oncology, Cedars-Sinai Medical Center, University of California Los Angeles (UCLA) School of Medicine, Los Angeles, California, United States of America ; Cancer Science Institute of Singapore and National Cancer Institute, National University of Singapore, Singapore, Singapore.
University of California, Los Angeles · USCedars-Sinai Medical Center · US

Funding

REGULATION OF HEMATOPOIETIC CYTOKINESR01CA026038 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI KOEFFLER, HAROLD PHILLIP · 1985 to 2013
$4.7M
MOLECULAR PATHOGENESIS OF CHLAMYDIA-INDUCED ATHEROGENESIR01HL066436 · NHLBI · CEDARS-SINAI MEDICAL CENTER · PI ARDITI, MOSHE · 2001 to 2013
$3.6M
Regulating Cathelicidin Expression for Disease TherapyR01AI065604 · NIAID · OREGON STATE UNIVERSITY · PI GOMBART, ADRIAN FRIEDRICH · 2007 to 2011
$2.1M
NCI NIH HHS 2R01 CA026038-32NCI NIH HHS R01 CA026038NHLBI NIH HHS R01 HL066436NIAID NIH HHS 5R01AI65604-6NIAID NIH HHS R01 AI065604
6 · The paper itself

Abstract

The CCAAT/enhancer binding proteins (C/EBPs) are transcription factors involved in hematopoietic cell development and induction of several inflammatory mediators. C/EBPε is expressed only in myeloid cells including monocytes/macrophages. Atherosclerosis is an inflammatory disorder of the vascular wall and circulating immune cells such as monocytes/macrophages. Mice deficient in the low density lipoprotein (LDL) receptor (Ldlr-/-) fed on a high cholesterol diet (HCD) show elevated blood cholesterol levels and are widely used as models to study human atherosclerosis. In this study, we generated Ldlr and Cebpe double-knockout (llee) mice and compared their atherogenic phenotypes to Ldlr single deficient (llEE) mice after HCD. Macrophages from llee mice have reduced lipid uptake by foam cells and impaired phagokinetic motility in vitro compared to macrophages from llEE mice. Also, compared to llEE mice, llee mice have alterations of lipid metabolism, and reduced atheroma and obesity, particularly the males. Peritoneal macrophages of llee male mice have reduced mRNA expression of FABP4, a fatty acid binding protein implicated in atherosclerosis. Overall, our study suggests that the myeloid specific factor C/EBPε is involved in systemic lipid metabolism and that silencing of C/EBPε could decrease the development of atherosclerosis.

Indexed as

AnimalsAtherosclerosisCCAAT-Enhancer-Binding ProteinsCell MovementImmunohistochemistryMaleMiceMice, Inbred C57BLMice, KnockoutReceptors, LDLCCAAT-Enhancer-Binding ProteinsReceptors, LDL

Identifiers

PMID24489659
PMCPMC3904867
OpenAlexW2024942564

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.