Evidence map›Paper›PMID 32330138›Full record

ArticlePloS one2020

Periostin interaction with discoidin domain receptor-1 (DDR1) promotes cartilage degeneration.

Tianzhen Han, Paolo Mignatti, Steven B Abramson, Mukundan Attur

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. 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
4.4field-weighted citation impact, top 5% 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

25 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  10. Periostin regulation and cartilage degradation early after anterior cruciate ligament reconstruction.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  11. Article
  12. Review
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  15. Periostin: an emerging activator of multiple signaling pathways.Journal of cell communication and signaling · 2022
    Review
  16. Article
  17. 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

4 authors at 1 institution in 1 country.

Tianzhen HanDivision of Rheumatology, Department of Medicine, NYU Grossman School of Medicine, NYU Langone Orthopedic Hospital, New York, NY, United States of America.
Paolo MignattiDivision of Rheumatology, Department of Medicine, NYU Grossman School of Medicine, NYU Langone Orthopedic Hospital, New York, NY, United States of America.
Steven B AbramsonDivision of Rheumatology, Department of Medicine, NYU Grossman School of Medicine, NYU Langone Orthopedic Hospital, New York, NY, United States of America.
Mukundan AtturDivision of Rheumatology, Department of Medicine, NYU Grossman School of Medicine, NYU Langone Orthopedic Hospital, New York, NY, United States of America.ORCID 0000-0001-7080-8118
New York University Langone Orthopedic Hospital · US

Funding

Regulation of chondrocytes by extracellular matrix protein.R01AR054817 · NIAMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ABRAMSON, STEVEN B · 2009 to 2014
$2.1M
The role of MT1-MMP proteolytic activity in osteogenesisR21AR070934 · NIAMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI MIGNATTI, PAOLO · 2017 to 2018
$410k
NIAMS NIH HHS R01 AR054817NIAMS NIH HHS R21 AR070934
6 · The paper itself

Abstract

Osteoarthritis (OA) is characterized by progressive loss of articular cartilage accompanied by the new bone formation and, often, a synovial proliferation that culminates in pain, loss of joint function, and disability. However, the cellular and molecular mechanisms of OA progression and the relative contributions of cartilage, bone, and synovium remain unclear. We recently found that the extracellular matrix (ECM) protein periostin (Postn, or osteoblast-specific factor, OSF-2) is expressed at high levels in human OA cartilage. Multiple groups have also reported elevated expression of Postn in several rodent models of OA. We have previously reported that in vitro Postn promotes collagen and proteoglycan degradation in human chondrocytes through AKT/β-catenin signaling and downstream activation of MMP-13 and ADAMTS4 expression. Here we show that Postn induces collagen and proteoglycan degradation in cartilage by signaling through discoidin domain receptor-1 (DDR1), a receptor tyrosine kinase. The genetic deficiency or pharmacological inhibition of DDR1 in mouse chondrocytes blocks Postn-induced MMP-13 expression. These data show that Postn is signaling though DDR1 is mechanistically involved in OA pathophysiology. Specific inhibitors of DDR1 may provide therapeutic opportunities to treat OA.

Indexed as

AgedAnimalsCartilage, ArticularCartilage DiseasesCell Adhesion MoleculesCells, CulturedChondrocytesDiscoidin Domain Receptor 1FemaleHumansMaleMatrix Metalloproteinase 13MiceMice, Inbred C57BLMice, KnockoutMiddle AgedCell Adhesion MoleculesDDR1 protein, humanDiscoidin Domain Receptor 1Matrix Metalloproteinase 13POSTN protein, human

Identifiers

PMID32330138
PMCPMC7182230
OpenAlexW3019541949

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.