Evidence map›Paper›PMID 15579451›Full record

ArticleThe American journal of pathology2004

Thrombospondin 2 functions as an endogenous regulator of angiogenesis and inflammation in rheumatoid arthritis.

Yong Wook Park, Young Mo Kang, Joe Butterfield, Michael Detmar, Jörg J Goronzy, Cornelia M Weyand

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

37 citing papers in PubMed, 97 citations in OpenAlex.

  1. Article
  2. CD105Breast cancer research : BCR · 2025
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  16. Thrombospondin-2 and extracellular matrix assembly.Biochimica et biophysica acta · 2014
    Review
  17. Review
  18. Review
  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

6 authors at 2 institutions in 1 country.

Yong Wook ParkDepartment of Medicine, Lowance Center for Human Immunology, Emory University School of Medicine, Atlanta, GA 30322, USA.
Young Mo Kang
Joe Butterfield
Michael Detmar
Jörg J Goronzy
Cornelia M Weyand
Emory University · USHarvard University · US

Funding

Oligoclonal T Cell Expansion &Rheumatoid ArthritisR01AR042527 · NIAMS · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 1993 to 2022
$4.8M
CD8 T CELLS IN RHEUMATOID SYNOVITISR01AI044142 · NIAID · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 1999 to 2010
$2.9M
OCULAR DISEASE IN GIANT CELL ARTERITISR01EY011916 · NEI · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 1997 to 2011
$2.9M
DIVERSITY OF T LYMPHOCYTES IN RHEUMATOID ARTHRITISR01AR041974 · NIAMS · MAYO CLINIC COLL OF MEDICINE, ROCHESTER · PI GORONZY, JORG J. · 1994 to 2006
$2.1M
NEI NIH HHS R01 EY011916NEI NIH HHS R01 EY 11916NIAID NIH HHS R01 AI044142NIAID NIH HHS R01 AI 44142NIAMS NIH HHS R01 AR041974NIAMS NIH HHS R01 AR042527NIAMS NIH HHS R01 AR 41974NIAMS NIH HHS R01 AR 42527
6 · The paper itself

Abstract

Thrombospondin 2 (TSP2), a matricellular protein with a primary role in modulating cell-matrix interactions, has been implicated in tissue repair and foreign body responses. Here we show that TSP2 has regulatory function in the chronic inflammatory lesions of rheumatoid arthritis. Tissue TSP2, produced by synovial fibroblasts, endothelial cells, and macrophages correlated not only with the intensity of angiogenesis but also with the architecture of lymphoid infiltrates. Synovial tissues with diffuse inflammatory infiltrates had high levels of TSP2, whereas synovial tissues with ectopic germinal center reactions and T cell-B cell aggregates produced low levels. Cell-based gene therapy with TSP2 was used to examine the in vivo effects of the matrix protein on neoangiogenesis and lymphoid organization. Human synovium-severe combined immunodeficiency (SCID) mouse chimeras were treated with TSP2-transfected fibroblasts deposited into the peritoneum. Overexpression of TSP2 led to the accumulation of TSP2 protein in the inflamed synovium and resulted in a prompt inhibition of lesional vascularization. Beside its anti-angiogenic activity, TSP2 also suppressed the production of the proinflammatory mediators, interferon-gamma and tumor necrosis factor-alpha, and induced the depletion of tissue-residing T cells. We propose that TSP2 is an endogenous regulator of angiogenesis and autoimmune inflammation in the synovium and represents a protective mechanism preventing ectopic lympho-organogenesis and persistent inflammation in this tissue site.

Indexed as

Neovascularization, PathologicAnimalsArthritis, RheumatoidB-LymphocytesCells, CulturedEndothelial CellsFibroblastsInflammationInterferon-gammaMacrophagesMiceMice, Inbred NODMice, SCIDPeritoneumSynovial MembraneSynovitisInterferon-gammaThrombospondin 2ThrombospondinsTumor Necrosis Factor-alpha

Identifiers

PMID15579451
PMCPMC1618704
OpenAlexW2060801600

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.