Evidence map›Paper›PMID 19443843›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2009

Cardiovascular inflammation and lesion cell apoptosis: a novel connection via the interferon-inducible immunoproteasome.

Zhaoqing Yang, Dmitry Gagarin, Georges St Laurent, Neil Hammell, Ian Toma, Chien-An Hu, Ayaka Iwasa, Timothy A McCaffrey

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
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  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. The role of interferon-γ in cardiovascular disease: an update.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020
    Review
  11. The Role of Deubiquitinases in Vascular Diseases.Journal of cardiovascular translational research · 2020
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. 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

8 authors at 2 institutions in 1 country.

Zhaoqing YangThe George Washington Medical Center, Department of Biochemistry and Molecular Biology, 2300 I Street NW, Ross Hall 541, Washington, DC 20037, USA.
Dmitry Gagarin
Georges St Laurent
Neil Hammell
Ian Toma
Chien-An Hu
Ayaka Iwasa
Timothy A McCaffrey
University of New Mexico · USGeorgetown University Medical Center · US

Funding

TGF-BETA 1 RECEPTORS IN RESTENOSIS AND AGINGR37AG012712 · NIA · GEORGE WASHINGTON UNIVERSITY · PI MCCAFFREY, TIMOTHY A. · 2001 to 2009
$2.9M
TGF-B1 RECEPTORS IN RESTENOSIS AND AGINGR01AG012712 · NIA · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI MCCAFFREY, TIMOTHY A. · 1996 to 2000
$403k
NIA NIH HHS AG12712NIA NIH HHS R01 AG012712NIA NIH HHS R37 AG012712
6 · The paper itself

Abstract

objectiveIncreasing evidence suggests that chronic inflammation contributes to atherogenesis, and that acute inflammatory events cause plaque rupture, thrombosis, and myocardial infarction. The present studies examined how inflammatory factors, such as interferon-gamma (IFNgamma), cause increased sensitivity to apoptosis in vascular lesion cells. METHODS AND

resultsCells from the fibrous cap of human atherosclerotic lesions were sensitized by interferon-gamma (IFNgamma) to Fas-induced apoptosis, in a Bcl-X(L) reversible manner. Microarray profiling identified 72 INFgamma-induced transcripts with potential relevance to apoptosis. Half could be excluded because they were induced by IRF-1 overexpression, which did not sensitize to apoptosis. IFNgamma treatment strongly reduced Mcl-1, phospho-Bcl-2 (ser70), and phospho-Bcl-X(L) (ser62) protein levels. Candidate transcripts were modulated by siRNA, overexpression, or inhibitors to assess the effect on IFNgamma-induced Fas sensitivity. Surprisingly, siRNA knockdown of PSMB8 (LMP7), an "immunoproteasome" component, reversed IFNgamma-induced sensitivity to Fas ligation and prevented Fas/IFNgamma-induced degradation of Mcl-1, but did not protect p-Bcl-2 or p-Bcl-X(L). Proteasome inhibition markedly increased Mcl-1, p-Bcl-2, and p-Bcl-X(L) levels after IFNgamma treatment.

conclusionsAlthough critical for antigen presentation, the immunoproteasome appears to be a key link between inflammatory factors and the control of vascular cell apoptosis and may thus be an important factor in plaque rupture and myocardial infarction.

Indexed as

Transcription, GeneticApoptosisAtherosclerosisbcl-X ProteinBlotting, WesternCarotid ArteriesCells, CulturedGene Expression RegulationHumansInterferon-gammaMultienzyme ComplexesProteasome Endopeptidase ComplexProto-Oncogene Proteins c-bcl-2Reverse Transcriptase Polymerase Chain ReactionRNA, Small InterferingSTAT1 Transcription Factorbcl-X ProteinInterferon-gammaLMP7 proteinMultienzyme ComplexesProteasome Endopeptidase ComplexProto-Oncogene Proteins c-bcl-2RNA, Small InterferingSTAT1 protein, humanSTAT1 Transcription Factor

Identifiers

PMID19443843
PMCPMC2762196
OpenAlexW2076493816

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.