Evidence map›Paper›PMID 18818413›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2008

Athsq1 is an atherosclerosis modifier locus with dramatic effects on lesion area and prominent accumulation of versican.

Sara Bretschger Seidelmann, Chaoling Kuo, Nick Pleskac, Jennifer Molina, Scott Sayers, Rong Li, Jing Zhou, Pamela Johnson, Kathleen Braun, Christina Chan and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.9field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. A role for proteoglycans in vascular disease.Matrix biology : journal of the International Society for Matrix Biology · 2018
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  17. Synthesis and organization of hyaluronan and versican by embryonic stem cells undergoing embryoid body differentiation.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2010
    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

15 authors at 1 institution.

Sara Bretschger SeidelmannDepartment of Medicine, Columbia University, New York, NY 10032, USA.
Chaoling Kuo
Nick Pleskac
Jennifer Molina
Scott Sayers
Rong Li
Jing Zhou
Pamela Johnson
Kathleen Braun
Christina Chan
Daniel Teupser
Jan L Breslow
Thomas N Wight
Alan R Tall
Carrie L Welch
Benaroya Research Institute

Funding

VLA-4 and VCAM-1 in Advanced AtherosclerosisP01HL018645 · NHLBI · UNIVERSITY OF WASHINGTON · PI CHAIT, ALAN · 1985 to 2010
$23.9M
Regulation and function of plasma lipid transfer proteinsP01HL054591 · NHLBI · ROCKEFELLER UNIVERSITY · PI GOLDBERG, IRA J · 1995 to 2010
$19.9M
NHLBI NIH HHS P01 HL018645NHLBI NIH HHS P01 HL054591
6 · The paper itself

Abstract

objectiveSusceptibility to atherosclerosis is genetically complex, and modifier genes that do not operate via traditional risk factors are largely unknown. A mouse genetics approach can simplify the genetic analysis and provide tools for mechanistic studies. METHODS AND

resultsWe previously identified atherosclerosis susceptibility QTL (Athsq1) on chromosome 4 acting independently of systemic risk factors. We now report confirmation of this locus in congenic strains carrying the MOLF-derived susceptibility allele in the C57BL/6J-Ldlr(-/-) genetic background. Homozygous congenic mice exhibited up to 4.5-fold greater lesion area compared to noncongenic littermates (P<0.0001). Analysis of extracellular matrix composition revealed prominent accumulation of versican, a presumed proatherogenic matrix component abundant in human lesions but almost absent in the widely-used C57BL/6 murine atherosclerosis model. The results of a bone marrow transplantation experiment suggested that both accelerated lesion development and versican accumulation are mediated, at least in part, by macrophages. Interestingly, comparative mapping revealed that the Athsq1 congenic interval contains the mouse region homologous to a widely-replicated CHD locus on human chromosome 9p21.

conclusionsThese studies confirm the proatherogenic activity of a novel gene(s) in the MOLF-derived Athsq1 locus and provide in vivo evidence for a causative role of versican in lesion development.

Indexed as

Quantitative Trait LociAnimalsAtherosclerosisBone Marrow TransplantationDisease Models, AnimalFemaleGenetic Predisposition to DiseaseHomozygoteHumansMaleMiceMice, CongenicMice, Inbred C57BLMice, KnockoutReceptors, LDLRNA, MessengerReceptors, LDLRNA, MessengerVcan protein, mouseVersicans

Identifiers

PMID18818413
PMCPMC2784896
OpenAlexW2152164512

What OpenQuestion holds

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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.