Evidence map›Paper›PMID 21477221›Full record

ArticleJournal of cellular and molecular medicine2011

Npp1 promotes atherosclerosis in ApoE knockout mice.

Yvonne Nitschke, Gabriele Weissen-Plenz, Robert Terkeltaub, Frank Rutsch

Open access · greenAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 44 citations in OpenAlex.

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  10. ABCC6, Pyrophosphate and Ectopic Calcification: Therapeutic Solutions.International journal of molecular sciences · 2021
    Review
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  20. Genetic pathways of vascular calcification.Trends in cardiovascular medicine · 2012
    Review
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

4 authors at 3 institutions in 2 countries.

Yvonne NitschkeDepartment of General Pediatrics, Muenster University Children's Hospital, Muenster, Germany.
Gabriele Weissen-Plenz
Robert Terkeltaub
Frank Rutsch
University Hospital Münster · DELeibniz Association · DEUniversity of California, San Diego · US

Funding

NPP1 and Molecular Mechanisms in Artery CalcificationR01HL077360 · NHLBI · VETERANS MEDICAL RESEARCH FDN/SAN DIEGO · PI TERKELTAUB, ROBERT A. · 2004 to 2012
$2.2M
Transglutaminase 2 in Arterial Calcification and AtherosclerosisR01HL087252 · NHLBI · VETERANS MEDICAL RESEARCH FDN/SAN DIEGO · PI TERKELTAUB, ROBERT A. · 2008 to 2011
$1.4M
NHLBI NIH HHS HL077360NHLBI NIH HHS HL087252NHLBI NIH HHS R01 HL077360NHLBI NIH HHS R01 HL087252
6 · The paper itself

Abstract

Ecto-nucleotide pyrophosphatase/phosphodiesterase 1 (NPP1) generates inorganic pyrophosphate (PP(i)), a physiologic inhibitor of hydroxyapatite deposition. In a previous study, we found NPP1 expression to be inversely correlated with the degree of atherosclerotic plaque calcification. Moreover, function-impairing mutations of ENPP1, the gene encoding for NPP1, are associated with severe, artery tunica media calcification and myointimal hyperplasia with infantile onset in human beings. NPP1 and PP(i) have the potential to modulate atherogenesis by regulating arterial smooth muscle cell (SMC) differentiation and function, including increase of pro-atherogenic osteopontin (OPN) expression. Hence, this study tested the hypothesis that NPP1 deficiency modulates both atherogenesis and atherosclerotic intimal plaque calcification. Npp1/ApoE double deficient mice were generated by crossing mice bearing the ttw allele of Enpp1 (that encodes a truncation mutation) with ApoE null mice and fed with high-fat/high-cholesterol atherogenic diet. Atherosclerotic lesion area and calcification were examined at 13, 18, 23 and 28 weeks of age. The aortic SMCs isolated from both ttw/ttw ApoE(-/-) and ttw/+ ApoE(-/-) mice demonstrated decreased Opn expression. The 28-week-old ttw/ttw ApoE(-/-) and ttw/+ ApoE(-/-) had significantly smaller atherosclerotic lesions compared with wild-type congenic ApoE(-/-) mice. Only ttw/ttw but not ttw/+ mice developed artery media calcification. Furthermore in ttw/+ mice, there was a tendency towards increased plaque calcification compared to ApoE(-/-) mice without Npp1 deficiency. We conclude that Npp1 promotes atherosclerosis, potentially mediated by Opn expression in ApoE knockout mice.

Indexed as

AnimalsApolipoproteins EArteriesAtherosclerosisBody WeightCalcinosisCells, CulturedLipidsMiceMice, Inbred ICRMice, KnockoutMuscle, Smooth, VascularMutationOsteopontinPhosphoric Diester HydrolasesPlaque, AtheroscleroticApolipoproteins Eectonucleotide pyrophosphatase phosphodiesterase 1LipidsOsteopontinPhosphoric Diester HydrolasesPyrophosphatases

Identifiers

PMID21477221
PMCPMC3154990
OpenAlexW2014318309

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.