Evidence map›Paper›PMID 11930008›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2002

Osteopontin deficiency protects joints against destruction in anti-type II collagen antibody-induced arthritis in mice.

Kenji Yumoto, Muneaki Ishijima, Susan R Rittling, Kunikazu Tsuji, Yoko Tsuchiya, Shigeyuki Kon, Akira Nifuji, Toshimitsu Uede, David T Denhardt, Masaki Noda

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
10.1field-weighted citation impact, top 1% 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

71 citing papers in PubMed, 206 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Kaempferol-A Natural Drug for Rheumatoid Arthritis.Chinese journal of integrative medicine · 2025
    Review
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  10. A Decreased Absolute Number of TAdvances in therapy · 2022
    Article
  11. Review
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  15. Article
  16. Article
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  18. Review
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11 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

10 authors at 3 institutions in 2 countries.

Kenji YumotoDepartment of Molecular Pharmacology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo 101-0062, Japan.
Muneaki Ishijima
Susan R Rittling
Kunikazu Tsuji
Yoko Tsuchiya
Shigeyuki Kon
Akira Nifuji
Toshimitsu Uede
David T Denhardt
Masaki Noda
Rutgers, The State University of New Jersey · USHokkaido University · JPTokyo Medical and Dental University · JP

Funding

REGULATIONN OF NO SYNTHESIS AND TOXICITY BY OSTEOPONTINP01ES006897 · NIEHS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI LASKIN, JEFFREY D · 1997 to 2001
$2.2M
OSTEOPONTIN SIGNALING--MECHANISM AND CONSEQUENCESR01AR044434 · NIAMS · RUTGERS THE ST UNIV OF NJ NEW BRUNSWICK · PI DENHARDT, DAVID T · 1997 to 2000
$264k
TUMORIGENESIS IN MICE LACKING OSTEOPONTINR01CA072740 · NCI · RUTGERS THE ST UNIV OF NJ NEW BRUNSWICK · PI RITTLING, SUSAN R · 1997 to 1999
–
NCI NIH HHS CA72740NIAMS NIH HHS AR44434NIEHS NIH HHS ES06897
6 · The paper itself

Abstract

Rheumatoid arthritis is one of the most critical diseases that impair the quality of life of patients, but its pathogenesis has not yet been fully understood. Osteopontin (OPN) is an extracellular matrix protein containing Arg-Gly-Asp (RGD) sequence, which interacts with alpha(v)beta3 integrins, promotes cell attachment, and cell migration and is expressed in both synovial cells and chondrocytes in rheumatoid arthritis; however, its functional relationship to arthritis has not been known. Therefore, we investigated the roles of OPN in the pathogenesis of inflammatory process in a rheumatoid arthritis model induced by a mixture of anti-type II collagen mAbs and lipopolysaccharide (mAbs/LPS). mAbs/LPS injection induced OPN expression in synovia as well as cartilage, and this expression was associated with joint swelling, destruction of the surface structures of the joint based on scanning electron microscopy, and loss of toluidine blue-positive proteoglycan content in the articular cartilage in wild-type mice. In contrast, OPN deficiency prevented the mice from such surface destruction, loss of proteoglycan in the articular joint cartilage, and swelling of the joints even when the mice were subjected to mAbs/LPS injection. Furthermore, mAbs/LPS injection in wild-type mice enhanced the levels of CD31-positive vessels in synovia and terminal deoxynucleotidyltransferase-mediated UTP end labeling-positive chondrocytes in the articular cartilage, whereas such angiogenesis as well as chondrocyte apoptosis was suppressed significantly in OPN-deficient mice. These results indicated that OPN plays a critical role in the destruction of joint cartilage in the rheumatoid arthritis model in mice via promotion of angiogenesis and induction of chondrocyte apoptosis.

Indexed as

AnimalsApoptosisArthritisCartilage, ArticularChondrocytesCollagen Type IILipopolysaccharidesMiceMice, Inbred C57BLNeovascularization, PathologicOsteopontinSialoglycoproteinsTumor Necrosis Factor-alphaCollagen Type IILipopolysaccharidesOsteopontinSialoglycoproteinsSpp1 protein, mouseTumor Necrosis Factor-alpha

Identifiers

PMID11930008
PMCPMC123686
OpenAlexW2159901127

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.