Evidence map›Paper›PMID 20068018›Full record

ArticleLupus2010

Lupus-prone New Zealand Black/New Zealand White F1 mice display endothelial dysfunction and abnormal phenotype and function of endothelial progenitor cells.

S G Thacker, D Duquaine, J Park, M J Kaplan

Open access · greenAbstract read
In one paragraph

Article in Lupus, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

42 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
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  9. Type-I interferons in atherosclerosis.The Journal of experimental medicine · 2020
    Review
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  14. Article
  15. Review
  16. Review
  17. Understanding mechanisms of hypertension in systemic lupus erythematosus.Therapeutic advances in cardiovascular disease · 2016
    Review
  18. Article
  19. Article
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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

4 authors at 1 institution in 1 country.

S G ThackerDivision of Rheumatology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109-5680, USA.
D Duquaine
J Park
M J Kaplan
University of Michigan–Ann Arbor · US

Funding

XenograftP30CA046592 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI THEODORE S LAWRENCE · 1988 to 2026
$178.2M
RESEARCH TRAINING IN EXPERIMENTAL IMMUNOPATHOLOGYT32AI007413 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Bethany B. Moore · 1993 to 2026
$9.8M
Vector CoreP30AR048310 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI TODD, ROBERT F · 2001 to 2010
$5.9M
NETs in the development of lupus and its cardiovascular complicationsR01HL088419 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI EITZMAN, DANIEL T · 2009 to 2016
$3.1M
NCI NIH HHS P30 CA046592NCI NIH HHS P30 CA46592NHLBI NIH HHS 5R01 HL088419-02NHLBI NIH HHS R01 HL088419NIAID NIH HHS T32 AI007413NIAID NIH HHS T32 AI07413NIAMS NIH HHS P30 AR048310NIAMS NIH HHS P30 AR48310
6 · The paper itself

Abstract

Patients with systemic lupus erythematosus (SLE) have an impairment in phenotype and function of endothelial progenitor cells (EPCs) which is mediated by interferon alpha (IFN-alpha). We assessed whether murine lupus models also exhibit vasculogenesis abnormalities and their potential association with endothelial dysfunction. Phenotype and function of EPCs and type I IFN gene signatures in EPC compartments were assessed in female New Zealand Black/New Zealand White F(1) (NZB/W), B6.MRL-Fas(lpr)/J (B6/lpr) and control mice. Thoracic aorta endothelial and smooth muscle function were measured in response to acetylcholine or sodium nitropruside, respectively. NZB/W mice displayed reduced numbers, increased apoptosis and impaired function of EPCs. These abnormalities correlated with significant decreases in endothelium-dependent vasomotor responses and with increased type I IFN signatures in EPC compartments. In contrast, B6/lpr mice showed improvement in endothelium-dependent and endothelial-independent responses, no abnormalities in EPC phenotype or function and downregulation of type I IFN signatures in EPC compartments. These results indicate that NZB/W mice represent a good model to study the mechanisms leading to endothelial dysfunction and abnormal vasculogenesis in lupus. These results further support the hypothesis that type I IFNs may play an important role in premature vascular damage and, potentially, atherosclerosis development in SLE.

Indexed as

AcetylcholineAnimalsAorta, ThoracicApoptosisDisease Models, AnimalDown-RegulationEndothelium, VascularFemaleInterferon-alphaInterferon Type ILupus Erythematosus, SystemicMiceMice, Inbred NZBNitroprussidePhenotypeStem CellsAcetylcholineInterferon-alphaInterferon Type INitroprussideVasodilator Agents

Identifiers

PMID20068018
PMCPMC3151666
OpenAlexW2042214412

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.