Evidence map›Paper›PMID 30212683›Full record

ArticleAtherosclerosis2018

Progranulin in the hematopoietic compartment protects mice from atherosclerosis.

Andrew D Nguyen, Thi A Nguyen, Rajesh K Singh, Delphine Eberlé, Jiasheng Zhang, Jess Porter Abate, Anatalia Robles, Suneil Koliwad, Eric J Huang, Frederick R Maxfield and 2 more

Open access · greenAbstract read
In one paragraph

Article in Atherosclerosis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. Article
  6. Review
  7. Adipokines, adiposity, and atherosclerosis.Cellular and molecular life sciences : CMLS · 2022
    Review
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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

12 authors at 6 institutions in 1 country.

Andrew D NguyenDepartment of Genetics and Complex Diseases, Harvard T. H. Chan School of Public Health, Boston, MA, 02115, USA; Department of Cell Biology, Harvard Medical School, Boston, MA, 02115, USA.
Thi A NguyenDepartment of Genetics and Complex Diseases, Harvard T. H. Chan School of Public Health, Boston, MA, 02115, USA; Department of Cell Biology, Harvard Medical School, Boston, MA, 02115, USA; Gladstone Institute of Cardiovascular Disease, San Francisco, CA, 94158, USA.
Rajesh K SinghDepartment of Biochemistry, Weill Cornell Medical College, New York, NY, 10065, USA.
Delphine EberléGladstone Institute of Cardiovascular Disease, San Francisco, CA, 94158, USA.
Jiasheng ZhangDepartment of Pathology, University of California, San Francisco, CA, 94143, USA; Pathology Service 113B, VA Medical Center, San Francisco, CA, 94121, USA.
Jess Porter AbateDiabetes Center, University of California, San Francisco, CA, 94143, USA.
Anatalia RoblesGladstone Histology Core, San Francisco, CA, 94158, USA.
Suneil KoliwadDiabetes Center, University of California, San Francisco, CA, 94143, USA.
Eric J HuangDepartment of Pathology, University of California, San Francisco, CA, 94143, USA; Pathology Service 113B, VA Medical Center, San Francisco, CA, 94121, USA; Bluefield Project to Cure FTD, San Francisco, CA, 94107, USA.
Frederick R MaxfieldDepartment of Biochemistry, Weill Cornell Medical College, New York, NY, 10065, USA.
Tobias C WaltherDepartment of Genetics and Complex Diseases, Harvard T. H. Chan School of Public Health, Boston, MA, 02115, USA; Department of Cell Biology, Harvard Medical School, Boston, MA, 02115, USA; Bluefield Project to Cure FTD, San Francisco, CA, 94107, USA; Broad Institute, Cambridge, MA, 02142, USA; Howard Hughes Medical Institute, Boston, MA, 02115, USA. Electronic address: twalther@hsph.harvard.edu.
Robert V FareseDepartment of Genetics and Complex Diseases, Harvard T. H. Chan School of Public Health, Boston, MA, 02115, USA; Department of Cell Biology, Harvard Medical School, Boston, MA, 02115, USA; Bluefield Project to Cure FTD, San Francisco, CA, 94107, USA; Broad Institute, Cambridge, MA, 02142, USA. Electronic address: robert@hsph.harvard.edu.
Gladstone Institutes · USBroad Institute · USCornell University · USSan Francisco VA Medical Center · USUniversity of California, San Francisco · USHarvard University · US

Funding

PrPSc SPECIFIC INTERACTION WITH NOVEL PrP-Fc FUSION PROTEINSP50AG023501 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MILLER, BRUCE L · 2004 to 2018
$27.1M
UCSF Nutrition Obesity Research CenterP30DK098722 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CHRISTIAN VAISSE · 2015 to 2026
$14.6M
Macrophage-Lipoprotein InteractionsR01HL093324 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI MAXFIELD, FREDERICK R. · 2009 to 2025
$6.7M
EXTRAMULAR RESEARCH FACILITIES CONSTRUCTIONC06RR018928 · NCRR · J. DAVID GLADSTONE INSTITUTES · PI MAHLEY, ROBERT W. · 2003 to 2003
$2.1M
Role of Progranulin in Mediating the Anti-Inflammatory Property of High-Density LF32HL116197 · NHLBI · J. DAVID GLADSTONE INSTITUTES · PI NGUYEN, ANDREW D. · 2012 to 2014
$116k
Mechanisms of Progranulin Deficiency in Neuroinflammation and NeurodegenerationI01BX002978 · VA · VETERANS AFFAIRS MED CTR SAN FRANCISCO · PI HUANG, ERIC J · 2017 to 2020
–
BLRD VA I01 BX002978Howard Hughes Medical InstituteNCRR NIH HHS C06 RR018928NHLBI NIH HHS F32 HL116197NHLBI NIH HHS R01 HL093324NIA NIH HHS P50 AG023501NIDDK NIH HHS P30 DK098722
6 · The paper itself

Abstract

BACKGROUND AND

aimsProgranulin is a circulating protein that modulates inflammation and is found in atherosclerotic lesions. Here we determined whether inflammatory cell-derived progranulin impacts atherosclerosis development.

methodsLdlr

resultsAfter 10 weeks of high-fat diet feeding, both groups displayed similarly elevated plasma levels of cholesterol and triglycerides. Despite abundant circulating levels of progranulin, the size of atherosclerotic lesions in Tx-KO mice was increased by 47% in aortic roots and by 62% in whole aortas. Aortic root lesions in Tx-KO mice had increased macrophage content and larger necrotic cores, consistent with more advanced lesions. Progranulin staining was markedly reduced in the lesions of Tx-KO mice, indicating little or no uptake of circulating progranulin. Mechanistically, cultured progranulin-deficient macrophages exhibited increased lysosome-mediated exophagy of aggregated low-density lipoproteins resulting in increased cholesterol uptake and foam cell formation.

conclusionsWe conclude that hematopoietic progranulin deficiency promotes diet-induced atherosclerosis in Ldlr

Indexed as

AnimalsAortaAortic DiseasesAtherosclerosisBone Marrow TransplantationCells, CulturedDiet, High-FatDisease Models, AnimalFemaleFoam CellsGenetic Predisposition to DiseaseGranulinsLipidsLysosomesMacrophagesMice, Inbred C57BLGranulinsGrn protein, mouseLipidsProgranulinsReceptors, LDLAggregated LDLAtherosclerosisExophagyLysosomeMacrophageProgranulin

Identifiers

PMID30212683
PMCPMC6432779
OpenAlexW2889269713

What OpenQuestion holds

Textmetadata
LicenceTDM
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.