Evidence map›Paper›PMID 25464168›Full record

ArticleOsteoarthritis and cartilage2015

Lysophosphatidic acid mediates fibrosis in injured joints by regulating collagen type I biosynthesis.

L Wu, F A Petrigliano, K Ba, S Lee, J Bogdanov, D R McAllister, J S Adams, A K Rosenthal, B Van Handel, G M Crooks and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Osteoarthritis and cartilage, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

16 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Autotaxin/Lysophosphatidic Acid Axis: From Bone Biology to Bone Disorders.International journal of molecular sciences · 2022
    Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Pirfenidone reduces subchondral bone loss and fibrosis after murine knee cartilage injury.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2018
    Article
  14. Article
  15. Review
  16. Autotaxin-LPA receptor axis in the pathogenesis of lung diseases.International journal of clinical and experimental medicine · 2015
    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

12 authors at 5 institutions in 2 countries.

L WuDepartment of Orthopaedic Surgery, Orthopedic Hospital Research Center, David Geffen School of Medicine (DGSOM), University of California at Los Angeles, Los Angeles, CA 90095, USA. Electronic address: lingwu@mednet.ucla.edu.
F A PetriglianoDepartment of Orthopaedic Surgery, Orthopedic Hospital Research Center, David Geffen School of Medicine (DGSOM), University of California at Los Angeles, Los Angeles, CA 90095, USA. Electronic address: FPetrigliano@mednet.ucla.edu.
K BaDepartment of Orthopaedic Surgery, Orthopedic Hospital Research Center, David Geffen School of Medicine (DGSOM), University of California at Los Angeles, Los Angeles, CA 90095, USA; State Key Laboratory for Oral Diseases, West China School of Stomatology, Sichuan University, Chengdu, 610041, China. Electronic address: k.ba@msn.com.
S LeeDepartment of Orthopaedic Surgery, Orthopedic Hospital Research Center, David Geffen School of Medicine (DGSOM), University of California at Los Angeles, Los Angeles, CA 90095, USA. Electronic address: siyounglee@mednet.ucla.edu.
J BogdanovDepartment of Orthopaedic Surgery, Orthopedic Hospital Research Center, David Geffen School of Medicine (DGSOM), University of California at Los Angeles, Los Angeles, CA 90095, USA. Electronic address: j.bogdanov@ucla.edu.
D R McAllisterDepartment of Orthopaedic Surgery, Orthopedic Hospital Research Center, David Geffen School of Medicine (DGSOM), University of California at Los Angeles, Los Angeles, CA 90095, USA. Electronic address: dmcallister@mednet.ucla.edu.
J S AdamsDepartment of Orthopaedic Surgery, Orthopedic Hospital Research Center, David Geffen School of Medicine (DGSOM), University of California at Los Angeles, Los Angeles, CA 90095, USA; UCLA Broad Stem Cell Institute for Regenerative Medicine and Stem Cell Research, USA; UCLA Jonsson Comprehensive Cancer Center, USA. Electronic address: JSAdams@mednet.ucla.edu.
A K RosenthalDivision of Rheumatology, Department of Medicine, Medical College of Wisconsin, 9200 West Wisconsin Avenue, Milwaukee WI 53226, USA. Electronic address: Ann.Rosenthal@va.gov.
B Van HandelNovogenix Laboratories, LLC, Los Angeles, CA 90033, USA. Electronic address: bvanhandel@novogenixlabs.com.
G M CrooksUCLA Broad Stem Cell Institute for Regenerative Medicine and Stem Cell Research, USA; UCLA Jonsson Comprehensive Cancer Center, USA; Department of Pathology and Laboratory Medicine, DGSOM, UCLA, USA. Electronic address: GCrooks@mednet.ucla.edu.
Y LinState Key Laboratory for Oral Diseases, West China School of Stomatology, Sichuan University, Chengdu, 610041, China. Electronic address: yunfenglin@scu.edu.cn.
D EvseenkoDepartment of Orthopaedic Surgery, Orthopedic Hospital Research Center, David Geffen School of Medicine (DGSOM), University of California at Los Angeles, Los Angeles, CA 90095, USA; UCLA Broad Stem Cell Institute for Regenerative Medicine and Stem Cell Research, USA; UCLA Jonsson Comprehensive Cancer Center, USA. Electronic address: devseenko@mednet.ucla.edu.
University of California, Los Angeles · USMedical College of Wisconsin · USPhysioGenix (United States) · USSichuan University · CNUniversity of Colorado Cancer Center · US

Funding

Generation of human chondroprogenitor cells for cartilage restorationK01AR061415 · NIAMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI EVSEENKO, DENIS · 2011 to 2015
$581k
NIAMS NIH HHS K01 AR061415NIAMS NIH HHS K01AR061415
6 · The paper itself

Abstract

objectiveArticular cartilage is a highly specialized tissue which forms the surfaces in synovial joints. Full-thickness cartilage defects caused by trauma or microfracture surgery heal via the formation of fibrotic tissue characterized by a high content of collagen I (COL I) and subsequent poor mechanical properties. The goal of this study is to investigate the molecular mechanisms underlying fibrosis after joint injury.

designRat knee joint models were used to mimic cartilage defects after acute injury. Immunohistochemistry was performed to detect proteins related to fibrosis. Human fetal chondrocytes and bone marrow stromal cells (BMSCs) were used to study the influence of the lipid lysophosphatidic acid (LPA) on COL I synthesis. Quantitative PCR, ELISA and immunohistochemistry were performed to evaluate the production of COL I. Chemical inhibitors were used to block LPA signaling both in vitro and in vivo.

resultsAfter full-thickness cartilage injury in rat knee joints, stromal cells migrating to the injury expressed high levels of the LPA-producing enzyme autotaxin (ATX); intact articular cartilage in rat and humans expressed negligible levels of ATX despite expressing the LPA receptors LPAR1 and LPAR2. LPA-induced increases in COL I production by chondrocytes and BMSCs were mediated by the MAP kinase and PI3 Kinase signaling pathways. Inhibition of the ATX/LPA axis significantly reduced COL I-enriched fibrocartilage synthesis in full-thickness cartilage defects in rats in favor of the collagen II-enriched normal state.

conclusionTaken together, these results identify an attractive target for intervention in reducing the progression of post-traumatic fibrosis and osteoarthritis.

Indexed as

AnimalsCartilage, ArticularCollagen Type IFibrosisHumansLysophospholipidsMaleRatsRats, Sprague-DawleyStifleCollagen Type Ilysophosphatidic acidLysophospholipidsAutotaxinCartilage injuryChondrocytesCollagen type IFibrosisLysophosphatidic acid

Identifiers

PMID25464168
PMCPMC4465392
OpenAlexW2097543161

What OpenQuestion holds

Textmetadata
LicenceTDM
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.