Evidence map›Paper›PMID 19900269›Full record

ArticleArthritis research & therapy2009

Insights in to the pathogenesis of axial spondyloarthropathy based on gene expression profiles.

Srilakshmi M Sharma, Dongseok Choi, Stephen R Planck, Christina A Harrington, Carrie R Austin, Jinnell A Lewis, Tessa N Diebel, Tammy M Martin, Justine R Smith, James T Rosenbaum

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.1field-weighted citation impact, top 14% 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, 56 citations in OpenAlex.

  1. Article
  2. Article
  3. TheBiomolecules · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Biomarker development for axial spondyloarthritis.Nature reviews. Rheumatology · 2020
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Srilakshmi M SharmaCasey Eye Institute, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, Oregon, 97239, USA. s_m_sharma@yahoo.com
Dongseok Choi
Stephen R Planck
Christina A Harrington
Carrie R Austin
Jinnell A Lewis
Tessa N Diebel
Tammy M Martin
Justine R Smith
James T Rosenbaum
Oregon Health & Science University · US

Funding

Proteomics CoreP30EY010572 · NEI · OREGON HEALTH & SCIENCE UNIVERSITY · PI TED S ACOTT · 1995 to 2026
$19.4M
UVEITIS GENE-EXPRESSOIN PROFILINGR01EY015858 · NEI · OREGON HEALTH & SCIENCE UNIVERSITY · PI ROSENBAUM, JAMES T · 2005 to 2008
$2.0M
NEI NIH HHS EY010572;NEI NIH HHS EY015858NEI NIH HHS P30 EY010572NEI NIH HHS R01 EY015858
6 · The paper itself

Abstract

introductionAxial spondyloarthropathy (SpA) is a group of inflammatory diseases, with ankylosing spondylitis as the prototype. SpA affects the axial skeleton, entheses, joints and, at times, the eyes. This study tested the hypothesis that SpA is characterized by a distinct pattern of gene expression in peripheral blood of affected individuals compared with healthy controls.

methodsHigh-density, human GeneChip probe arrays were used to profile mRNA of peripheral blood cells from 18 subjects with SpA and 25 normal individuals. Samples were processed as two separate sets at different times (11 SpA + 12 control subjects in primary set (Set 1); 7 SpA+ 13 control subjects in the validation set (Set 2)). Blood samples were taken at a time when patients were not receiving systemic immunomodulatory therapy. Differential expression was defined as a 1.5-fold change with a q value < 5%. Gene ontology and pathway information were also studied.

resultsSignals from 134 probe sets (representing 95 known and 12 unknown gene transcripts) were consistently different from controls in both Sets 1 and 2. Included among these were transcripts for a group of 20 genes, such as interleukin-1 (IL-1) receptors 1 and 2, Nod-like receptor family, pyrin domain containing 2 (NLRP2), secretory leukocyte peptidase inhibitor (SLPI), secreted protein acidic and rich in cysteine (SPARC), and triggering receptor expressed on myeloid cells 1 (TREM-1) that are clearly related to the immune or inflammatory response and a group of 4 transcripts that have a strong role in bone remodeling.

conclusionsOur observations are the first to implicate SPARC, SLPI, and NLRP2, a component of the innate immune system, in the pathogenesis of SpA. Our results also indicate a possible role for IL-1 and its receptors in SpA. In accord with the bone pathology component of SpA, we also found that expression levels of transcripts reflecting bone remodeling factors are also distinguishable in peripheral blood from patients with SpA versus controls. These results confirm some previously identified biomarkers implicated in the pathogenesis of SpA and also point to novel mediators in this disease.

Indexed as

Gene Expression ProfilingAdultBlood ProteinsFemaleGene ExpressionHumansMaleMembrane ProteinsMiddle AgedNerve Tissue ProteinsOligonucleotide Array Sequence AnalysisOsteonectinSpondylarthropathiesBlood ProteinsMembrane ProteinsNerve Tissue ProteinsOsteonectinSTOML1 protein, humanSTOML2 protein, human

Identifiers

PMID19900269
PMCPMC3003511
OpenAlexW2160433954

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.