Evidence map›Paper›PMID 11067863›Full record

ArticleThe Journal of clinical investigation2000

Apolipoprotein J/clusterin limits the severity of murine autoimmune myocarditis.

L McLaughlin, G Zhu, M Mistry, C Ley-Ebert, W D Stuart, C J Florio, P A Groen, S A Witt, T R Kimball, D P Witte and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
4.0field-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

78 citing papers in PubMed, 208 citations in OpenAlex.

  1. Article
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  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Clusterin, other extracellular chaperones, and eye disease.Progress in retinal and eye research · 2022
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article

18 more citing papers are in PubMed but not listed here.

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 4 institutions in 2 countries.

L McLaughlinDepartment of Pharmacology and Cell Biophysics, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267-0575, USA.
G Zhu
M Mistry
C Ley-Ebert
W D Stuart
C J Florio
P A Groen
S A Witt
T R Kimball
D P Witte
J A Harmony
B J Aronow
Institut thématique Génétique, génomique et bioinformatique · FRUniversity of Cincinnati Medical Center · USCincinnati Children's Hospital Medical Center · USEmory University Hospital · US

Funding

REGULATION OF AN EXTRACELLULAR XENOBIOTIC RESPONSE GENER01ES008822 · NIEHS · CHILDREN'S HOSPITAL MED CTR (CINCINNATI) · PI ARONOW, BRUCE J. · 1997 to 1999
–
NIEHS NIH HHS ES 08822
6 · The paper itself

Abstract

Apolipoprotein J/clusterin (apoJ/clusterin), an intriguing protein with unknown function, is induced in myocarditis and numerous other inflammatory injuries. To test its ability to modify myosin-induced autoimmune myocarditis, we generated apoJ-deficient mice. ApoJ-deficient and wild-type mice exhibited similar initial onset of myocarditis, as evidenced by the induction of two early markers of the T cell-mediated immune response, MHC-II and TNF receptor p55. Furthermore, autoantibodies against the primary antigen cardiac myosin were induced to the same extent. Although the same proportion of challenged animals exhibited some degree of inflammatory infiltrate, inflammation was more severe in apoJ-deficient animals. Inflammatory lesions were more diffuse and extensive in apoJ-deficient mice, particularly in females. In marked contrast to wild-type animals, the development of a strong generalized secondary response against cardiac antigens in apoJ-deficient mice was predictive of severe myocarditis. Wild-type mice with a strong Ab response to secondary antigens appeared to be protected from severe inflammation. After resolution of inflammation, apoJ-deficient, but not wild-type, mice exhibited cardiac function impairment and severe myocardial scarring. These results suggest that apoJ limits progression of autoimmune myocarditis and protects the heart from postinflammatory tissue destruction.

Indexed as

Molecular ChaperonesAnimalsAntigens, CDAutoantibodiesAutoimmune DiseasesBase SequenceClusterinDNA PrimersFemaleGlycoproteinsHistocompatibility Antigens Class IIMaleMiceMice, KnockoutMyocarditisMyosinsAntigens, CDAutoantibodiesClu protein, mouseClusterinDNA PrimersGlycoproteinsHistocompatibility Antigens Class IIMolecular ChaperonesMyosinsReceptors, Tumor Necrosis FactorReceptors, Tumor Necrosis Factor, Type I

Identifiers

PMID11067863
PMCPMC301413
OpenAlexW1986451738

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.