Evidence map›Paper›PMID 26061292›Full record

ArticlePloS one2015

LDL Receptor-Related Protein-1 (LRP1) Regulates Cholesterol Accumulation in Macrophages.

Anna P Lillis, Selen Catania Muratoglu, Dianaly T Au, Mary Migliorini, Mi-Jeong Lee, Susan K Fried, Irina Mikhailenko, Dudley K Strickland

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

36 citing papers in PubMed, 54 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Cellular crosstalk in atherosclerotic plaque microenvironment.Cell communication and signaling : CCS · 2023
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  7. The Endocannabinoid System in Caenorhabditis elegans.Reviews of physiology, biochemistry and pharmacology · 2023
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  8. Article
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  13. Synaptic tau: A pathological or physiological phenomenon?Acta neuropathologica communications · 2021
    Review
  14. Lysosomal Stress Response (LSR): Physiological Importance and Pathological Relevance.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2021
    Review
  15. Review
  16. Macrophage Plasticity and Atherosclerosis Therapy.Frontiers in molecular biosciences · 2021
    Review
  17. Article
  18. Article
  19. Article
  20. Immunization with the GlyTheranostics · 2020
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Anna P LillisCenter for Vascular and Inflammatory Diseases, University of Maryland School of Medicine, Baltimore, MD 21201, United States of America; Department of Pathology, Duke University Medical Center, Durham, NC 27710, United States of America.
Selen Catania MuratogluCenter for Vascular and Inflammatory Diseases, University of Maryland School of Medicine, Baltimore, MD 21201, United States of America; Department of Physiology, University of Maryland School of Medicine, Baltimore, MD 21201, United States of America.
Dianaly T AuCenter for Vascular and Inflammatory Diseases, University of Maryland School of Medicine, Baltimore, MD 21201, United States of America.
Mary MiglioriniCenter for Vascular and Inflammatory Diseases, University of Maryland School of Medicine, Baltimore, MD 21201, United States of America; Department of Surgery, University of Maryland School of Medicine, Baltimore, MD 21201, United States of America.
Mi-Jeong LeeDepartment of Medicine, Section of Endocrinology, Diabetes and Nutrition, Boston University School of Medicine, Boston, MA 02118, United States of America.
Susan K FriedDepartment of Medicine, Section of Endocrinology, Diabetes and Nutrition, Boston University School of Medicine, Boston, MA 02118, United States of America.
Irina MikhailenkoCenter for Vascular and Inflammatory Diseases, University of Maryland School of Medicine, Baltimore, MD 21201, United States of America; Department of Physiology, University of Maryland School of Medicine, Baltimore, MD 21201, United States of America.
Dudley K StricklandCenter for Vascular and Inflammatory Diseases, University of Maryland School of Medicine, Baltimore, MD 21201, United States of America; Department of Physiology, University of Maryland School of Medicine, Baltimore, MD 21201, United States of America; Department of Surgery, University of Maryland School of Medicine, Baltimore, MD 21201, United States of America.
University of Maryland, Baltimore · USBoston University · USDuke Medical Center · US

Funding

Research BaseP30DK072488 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI MITCHELL, BRAXTON D, TAYLOR, SIMEON I. · 2005 to 2019
$17.3M
Vascular Biology Training ProgramT32HL007698 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI Rosemary A Kozar, Dudley K. Strickland · 1991 to 2026
$8.7M
Role of Lipoprotein Receptors in Venous ThrombosisR01HL114379 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI STRICKLAND, DUDLEY K. · 2012 to 2016
$1.9M
Mechanisms by which LRP1 Protects the VasculatureR01HL120388 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI STRICKLAND, DUDLEY K. · 2014 to 2016
$1.1M
NHLBI NIH HHS R01 HL114379NHLBI NIH HHS R01 HL120388NHLBI NIH HHS T32 HL007698NIDDK NIH HHS P30 DK072488
6 · The paper itself

Abstract

Within the circulation, cholesterol is transported by lipoprotein particles and is taken up by cells when these particles associate with cellular receptors. In macrophages, excessive lipoprotein particle uptake leads to foam cell formation, which is an early event in the development of atherosclerosis. Currently, mechanisms responsible for foam cell formation are incompletely understood. To date, several macrophage receptors have been identified that contribute to the uptake of modified forms of lipoproteins leading to foam cell formation, but the in vivo contribution of the LDL receptor-related protein 1 (LRP1) to this process is not known [corrected]. To investigate the role of LRP1 in cholesterol accumulation in macrophages, we generated mice with a selective deletion of LRP1 in macrophages on an LDL receptor (LDLR)-deficient background (macLRP1-/-). After feeding mice a high fat diet for 11 weeks, peritoneal macrophages isolated from Lrp+/+ mice contained significantly higher levels of total cholesterol than those from macLRP1-/- mice. Further analysis revealed that this was due to increased levels of cholesterol esters. Interestingly, macLRP1-/- mice displayed elevated plasma cholesterol and triglyceride levels resulting from accumulation of large, triglyceride-rich lipoprotein particles in the circulation. This increase did not result from an increase in hepatic VLDL biosynthesis, but rather results from a defect in catabolism of triglyceride-rich lipoprotein particles in macLRP1-/- mice. These studies reveal an important in vivo contribution of macrophage LRP1 to cholesterol homeostasis.

Indexed as

Adipose TissueAnimalsCholesterolGene DeletionKupffer CellsLipaseLiverLow Density Lipoprotein Receptor-Related Protein-1MiceMice, TransgenicMusclesReceptors, LDLTumor Suppressor ProteinsCholesterolLipaseLow Density Lipoprotein Receptor-Related Protein-1Lrp1 protein, mouseReceptors, LDLTumor Suppressor Proteins

Identifiers

PMID26061292
PMCPMC4463855
OpenAlexW1509542786

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.