Evidence map›Paper›PMID 24289792›Full record

ArticleArthritis research & therapy2013

Impact of extracellular matrix derived from osteoarthritis subchondral bone osteoblasts on osteocytes: role of integrinβ1 and focal adhesion kinase signaling cues.

Indira Prasadam, Saba Farnaghi, Jian Q Feng, Wenyi Gu, Samuel Perry, Ross Crawford, Yin Xiao

Abstract read
In one paragraph

Article in Arthritis research & therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
–field-weighted citation impact
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

25 citing papers in PubMed.

  1. Article
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  8. Article
  9. Article
  10. Review
  11. Review
  12. Mechanistic Insight Into the Roles of Integrins in Osteoarthritis.Frontiers in cell and developmental biology · 2021
    Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
  19. Osteoblast role in osteoarthritis pathogenesis.Journal of cellular physiology · 2017
    Review
  20. Osteoblast Role in Rheumatic Diseases.International journal of molecular sciences · 2017
    Review
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

7 authors.

Indira Prasadam
Saba Farnaghi
Jian Q Feng
Wenyi Gu
Samuel Perry
Ross Crawford
Yin Xiao

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionOur recent study indicated that subchondral bone pathogenesis in osteoarthritis (OA) is associated with osteocyte morphology and phenotypic abnormalities. However, the mechanism underlying this abnormality needs to be identified. In this study we investigated the effect of extracellular matrix (ECM) produced from normal and OA bone on osteocytic cells function.

methodsDe-cellularized matrices, resembling the bone provisional ECM secreted from primary human subchondral bone osteoblasts (SBOs) of normal and OA patients were used as a model to study the effect on osteocytic cells. Osteocytic cells (MLOY4 osteocyte cell line) cultured on normal and OA derived ECMs were analyzed by confocal microscopy, scanning electron microscopy (SEM), cell attachment assays, zymography, apoptosis assays, qRT-PCR and western blotting. The role of integrinβ1 and focal adhesion kinase (FAK) signaling pathways during these interactions were monitored using appropriate blocking antibodies.

resultsThe ECM produced by OA SBOs contained less mineral content, showed altered organization of matrix proteins and matrix structure compared with the matrices produced by normal SBOs. Culture of osteocytic cells on these defective OA ECM resulted in a decrease of integrinβ1 expression and the de-activation of FAK cell signaling pathway, which subsequently affected the initial osteocytic cell's attachment and functions including morphological abnormalities of cytoskeletal structures, focal adhesions, increased apoptosis, altered osteocyte specific gene expression and increased Matrix metalloproteinases (MMP-2) and -9 expression.

conclusionThis study provides new insights in understanding how altered OA bone matrix can lead to the abnormal osteocyte phenotypic changes, which is typical in OA pathogenesis.

Indexed as

Signal TransductionAgedAnimalsApoptosisBlotting, WesternCell AdhesionCell LineCell ProliferationCells, CulturedExtracellular MatrixFocal Adhesion Protein-Tyrosine KinasesHumansImmunohistochemistryIntegrin beta1Matrix Metalloproteinase 2Matrix Metalloproteinase 9Focal Adhesion Protein-Tyrosine KinasesIntegrin beta1Matrix Metalloproteinase 2Matrix Metalloproteinase 9

Identifiers

PMID24289792
PMCPMC3978998

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Registered trials

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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.