Evidence map›Paper›PMID 26092928›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2015

Elevated expression of periostin in human osteoarthritic cartilage and its potential role in matrix degradation via matrix metalloproteinase-13.

Mukundan Attur, Qing Yang, Kohei Shimada, Yuki Tachida, Hiroyuki Nagase, Paolo Mignatti, Lauren Statman, Glyn Palmer, Thorsten Kirsch, Frank Beier and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 6% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Proteomics Reveals Increased Periostin in Synovial Fluid From Canine and Human Anterior Cruciate Ligament Injury.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2025
    Article
  4. A review of periostin in orthopedics.Osteoarthritis and cartilage open · 2025
    Review
  5. Research progress and prospect of MAPK signaling pathway in knee osteoarthritis.European journal of orthopaedic surgery & traumatology : orthopedie traumatologie · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. 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
  14. Article
  15. Review
  16. Article
  17. Article
  18. Periostin: an emerging activator of multiple signaling pathways.Journal of cell communication and signaling · 2022
    Review
  19. Article
  20. Article
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

11 authors at 4 institutions in 3 countries.

Mukundan Attur*Division of Rheumatology, Department of Medicine, Department of Cell Biology, and Department of Orthopaedic Surgery, New York University (NYU) School of Medicine and NYU Langone Medical Center, New York, New York, USA; Frontier Research Laboratories, Daiichi Sankyo Co., Ltd., Tokyo, Japan; Department of Orthopaedics and Rehabilitation, University of Florida, Gainesville, Florida, USA; and Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, Ontario, Canada mukundan.attur@nyumc.org.
Qing Yang*Division of Rheumatology, Department of Medicine, Department of Cell Biology, and Department of Orthopaedic Surgery, New York University (NYU) School of Medicine and NYU Langone Medical Center, New York, New York, USA; Frontier Research Laboratories, Daiichi Sankyo Co., Ltd., Tokyo, Japan; Department of Orthopaedics and Rehabilitation, University of Florida, Gainesville, Florida, USA; and Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, Ontario, Canada.
Kohei Shimada*Division of Rheumatology, Department of Medicine, Department of Cell Biology, and Department of Orthopaedic Surgery, New York University (NYU) School of Medicine and NYU Langone Medical Center, New York, New York, USA; Frontier Research Laboratories, Daiichi Sankyo Co., Ltd., Tokyo, Japan; Department of Orthopaedics and Rehabilitation, University of Florida, Gainesville, Florida, USA; and Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, Ontario, Canada.
Yuki Tachida*Division of Rheumatology, Department of Medicine, Department of Cell Biology, and Department of Orthopaedic Surgery, New York University (NYU) School of Medicine and NYU Langone Medical Center, New York, New York, USA; Frontier Research Laboratories, Daiichi Sankyo Co., Ltd., Tokyo, Japan; Department of Orthopaedics and Rehabilitation, University of Florida, Gainesville, Florida, USA; and Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, Ontario, Canada.
Hiroyuki Nagase*Division of Rheumatology, Department of Medicine, Department of Cell Biology, and Department of Orthopaedic Surgery, New York University (NYU) School of Medicine and NYU Langone Medical Center, New York, New York, USA; Frontier Research Laboratories, Daiichi Sankyo Co., Ltd., Tokyo, Japan; Department of Orthopaedics and Rehabilitation, University of Florida, Gainesville, Florida, USA; and Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, Ontario, Canada.
Paolo Mignatti*Division of Rheumatology, Department of Medicine, Department of Cell Biology, and Department of Orthopaedic Surgery, New York University (NYU) School of Medicine and NYU Langone Medical Center, New York, New York, USA; Frontier Research Laboratories, Daiichi Sankyo Co., Ltd., Tokyo, Japan; Department of Orthopaedics and Rehabilitation, University of Florida, Gainesville, Florida, USA; and Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, Ontario, Canada.
Lauren Statman*Division of Rheumatology, Department of Medicine, Department of Cell Biology, and Department of Orthopaedic Surgery, New York University (NYU) School of Medicine and NYU Langone Medical Center, New York, New York, USA; Frontier Research Laboratories, Daiichi Sankyo Co., Ltd., Tokyo, Japan; Department of Orthopaedics and Rehabilitation, University of Florida, Gainesville, Florida, USA; and Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, Ontario, Canada.
Glyn Palmer*Division of Rheumatology, Department of Medicine, Department of Cell Biology, and Department of Orthopaedic Surgery, New York University (NYU) School of Medicine and NYU Langone Medical Center, New York, New York, USA; Frontier Research Laboratories, Daiichi Sankyo Co., Ltd., Tokyo, Japan; Department of Orthopaedics and Rehabilitation, University of Florida, Gainesville, Florida, USA; and Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, Ontario, Canada.
Thorsten Kirsch*Division of Rheumatology, Department of Medicine, Department of Cell Biology, and Department of Orthopaedic Surgery, New York University (NYU) School of Medicine and NYU Langone Medical Center, New York, New York, USA; Frontier Research Laboratories, Daiichi Sankyo Co., Ltd., Tokyo, Japan; Department of Orthopaedics and Rehabilitation, University of Florida, Gainesville, Florida, USA; and Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, Ontario, Canada.
Frank Beier*Division of Rheumatology, Department of Medicine, Department of Cell Biology, and Department of Orthopaedic Surgery, New York University (NYU) School of Medicine and NYU Langone Medical Center, New York, New York, USA; Frontier Research Laboratories, Daiichi Sankyo Co., Ltd., Tokyo, Japan; Department of Orthopaedics and Rehabilitation, University of Florida, Gainesville, Florida, USA; and Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, Ontario, Canada.
Steven B Abramson*Division of Rheumatology, Department of Medicine, Department of Cell Biology, and Department of Orthopaedic Surgery, New York University (NYU) School of Medicine and NYU Langone Medical Center, New York, New York, USA; Frontier Research Laboratories, Daiichi Sankyo Co., Ltd., Tokyo, Japan; Department of Orthopaedics and Rehabilitation, University of Florida, Gainesville, Florida, USA; and Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, Ontario, Canada.
NYU Langone Health · USDaiichi-Sankyo (Japan) · JPUniversity of Florida · USWestern University · CA

Funding

Using social networks to map and evaluate team science across CTSA hubsUL1TR001427 · NCATS · UNIVERSITY OF FLORIDA · PI MITCHELL, DUANE A. · 2015 to 2024
$37.2M
NON-PROTEOLYTIC INTERACTIONS OF TIMP-2 AND MT1-MMPR01CA136715 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI MIGNATTI, PAOLO · 2009 to 2014
$2.3M
Regulation of chondrocytes by extracellular matrix protein.R01AR054817 · NIAMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ABRAMSON, STEVEN B · 2009 to 2014
$2.1M
NCATS NIH HHS UL1 TR001427NCI NIH HHS R01 CA136715NCI NIH HHS R01-CA136715NIAMS NIH HHS R01 AR054817NIAMS NIH HHS R01-AR054817
6 · The paper itself

Abstract

We investigated the role of periostin, an extracellular matrix protein, in the pathophysiology of osteoarthritis (OA). In OA, dysregulated gene expression and phenotypic changes in articular chondrocytes culminate in progressive loss of cartilage from the joint surface. The molecular mechanisms underlying this process are poorly understood. We examined periostin expression by immunohistochemical analysis of lesional and nonlesional cartilage from human and rodent OA knee cartilage. In addition, we used small interfering (si)RNA and adenovirus transduction of chondrocytes to knock down and up-regulate periostin levels, respectively, and analyzed its effect on matrix metalloproteinase (MMP)-13, a disintegrin and MMP with thrombospondin motifs (ADAMTS)-4, and type II collagen expression. We found high periostin levels in human and rodent OA cartilage. Periostin increased MMP-13 expression dose [1-10 µg/ml (EC50 0.5-1 μg/ml)] and time (24-72 h) dependently, significantly enhanced expression of ADAMTS4 mRNA, and promoted cartilage degeneration through collagen and proteoglycan degradation. Periostin induction of MMP-13 expression was inhibited by CCT031374 hydrobromide, an inhibitor of the canonical Wnt/β-catenin signaling pathway. In addition, siRNA-mediated knockdown of endogenous periostin blocked constitutive MMP-13 expression. These findings implicate periostin as a catabolic protein that promotes cartilage degeneration in OA by up-regulating MMP-13 through canonical Wnt signaling.

Indexed as

ADAM ProteinsADAMTS4 ProteinAgedAged, 80 and overAnimalsBlotting, WesternCartilage, ArticularCattleCell Adhesion MoleculesCells, CulturedChondrocytesDisease Models, AnimalExtracellular MatrixFemaleGene Expression ProfilingHumansADAM ProteinsADAMTS4 ProteinADAMTS4 protein, humanAdamts4 protein, mouseCell Adhesion MoleculesMatrix Metalloproteinase 13POSTN protein, humanProcollagen N-EndopeptidaseADAMTSchondrocytesposttraumatic osteoarthritisWnt signaling

Identifiers

PMID26092928
PMCPMC4566939
OpenAlexW2121702635

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.