Evidence map›Paper›PMID 27856294›Full record

ArticleOsteoarthritis and cartilage2017

Role of the C-C chemokine receptor-2 in a murine model of injury-induced osteoarthritis.

L Longobardi, J D Temple, L Tagliafierro, H Willcockson, A Esposito, N D'Onofrio, E Stein, T Li, T J Myers, H Ozkan and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Osteoarthritis and cartilage, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.5field-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

43 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Pharmacological antagonism of Ccr2+ cell recruitment to facilitate regenerative tendon healing.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2025
    Article
  3. Article
  4. Dietary supplementation of vitamin B1 prevents the pathogenesis of osteoarthritis.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 7 institutions in 3 countries.

L LongobardiDivision of Rheumatology, Allergy and Immunology and the Thurston Arthritis Research Center, University of North Carolina-Chapel Hill, NC, USA. Electronic address: lara_longobardi@med.unc.edu.
J D TempleDepartment of Biomedical Engineering, UNC-Chapel Hill, NC, USA; Department of Pediatrics, Rush University Medical Center, Chicago, IL, USA. Electronic address: Joseph_Temple@rush.edu.
L TagliafierroDepartment of Neurology, Duke University, Durham, NC, USA. Electronic address: lidiatag@hotmail.it.
H WillcocksonDepartment of Cell Biology and Physiology, UNC-Chapel Hill, NC, USA. Electronic address: helen_willcockson@med.unc.edu.
A EspositoDepartment of Pediatrics, Rush University Medical Center, Chicago, IL, USA. Electronic address: Alessandra_Esposito@rush.edu.
N D'OnofrioDepartment of Biochemistry, Biophysics and General Pathology, Second University of Naples, Naples, Italy. Electronic address: nunzia.donofrio@unina2.it.
E SteinDepartment of Pharmacology and Cancer Biology, Duke University, Durham, NC, USA. Electronic address: emstein90@gmail.com.
T LiDepartment of Pediatrics, Rush University Medical Center, Chicago, IL, USA. Electronic address: Tieshi_Li@rush.edu.
T J MyersDepartment of Pediatrics, UNC-Chapel Hill, NC, USA. Electronic address: timothymyers59@gmail.com.
H OzkanDepartment of Orthopaedics, Gulhane Military Medical Academy, Etlik, Ankara, Turkey. Electronic address: heorto@yahoo.com.
M L BalestrieriDepartment of Biochemistry, Biophysics and General Pathology, Second University of Naples, Naples, Italy. Electronic address: marialuisa.balestrieri@unina2.it.
V UliciDivision of Rheumatology, Allergy and Immunology and the Thurston Arthritis Research Center, University of North Carolina-Chapel Hill, NC, USA. Electronic address: verau79@yahoo.com.
R F LoeserDivision of Rheumatology, Allergy and Immunology and the Thurston Arthritis Research Center, University of North Carolina-Chapel Hill, NC, USA. Electronic address: richard_loeser@med.unc.edu.
A SpagnoliDepartment of Pediatrics, Rush University Medical Center, Chicago, IL, USA. Electronic address: Anna_Spagnoli@rush.edu.
University of North Carolina at Chapel Hill · USRush University Medical Center · USDuke University · USTurkish Armed Forces · TRUniversity of Campania "Luigi Vanvitelli" · ITUniversity of Naples Federico II · ITUniversity of North Carolina Health Care · US

Funding

Molecular Mechanisms in Joint DevelopmentR01AR057042 · NIAMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SPAGNOLI, ANNA · 2010 to 2014
$1.6M
MCP5 as key mediator of TGFbeta signaling in joint maintenance and osteoarthritisR03AR063232 · NIAMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI LONGOBARDI, LARA · 2012 to 2014
$217k
NIAMS NIH HHS R01 AR057042NIAMS NIH HHS R03 AR063232
6 · The paper itself

Abstract

objectiveWe previously found in our embryonic studies that proper regulation of the chemokine CCL12 through its sole receptor CCR2, is critical for joint and growth plate development. In the present study, we examined the role of CCR2 in injury-induced-osteoarthritis (OA).

methodWe used a murine model of injury-induced-OA (destabilization of medial meniscus, DMM), and systemically blocked CCR2 using a specific antagonist (RS504393) at different times during disease progression. We examined joint degeneration by assessing cartilage (cartilage loss, chondrocyte hypertrophy, MMP-13 expression) and bone lesions (bone sclerosis, osteophytes formation) with or without the CCR2 antagonist. We also performed pain behavioral studies by assessing the weight distribution between the normal and arthritic hind paws using the IITS incapacitance meter.

resultsTesting early vs delayed administration of the CCR2 antagonist demonstrated differential effects on joint damage. We found that OA changes in articular cartilage and bone were ameliorated by pharmacological CCR2 blockade, if given early in OA development: specifically, pharmacological targeting of CCR2 during the first 4 weeks (wks) following injury, reduced OA cartilage and bone damage, with less effectiveness with later treatments. Importantly, our pain-related behavioral studies showed that blockade of CCR2 signaling during early, 1-4 wks post-surgery or moderate, 4-8 wks post-surgery, OA was sufficient to decrease pain measures, with sustained improvement at later stages, after treatment was stopped.

conclusionsOur data highlight the potential efficacy of antagonizing CCR2 at early stages to slow the progression of post-injury OA and, in addition, improve pain symptoms.

Indexed as

AnimalsBenzoxazinesBone and BonesCartilage, ArticularChondrocytesDisease Models, AnimalDisease ProgressionHypertrophyMatrix Metalloproteinase 13Menisci, TibialMiceOsteoarthritisOsteophyteReceptors, CCR2SclerosisSpiro CompoundsBenzoxazinesCcr2 protein, mouseMatrix Metalloproteinase 13Mmp13 protein, mouseReceptors, CCR2RS 504393Spiro CompoundsAnimal modelBoneCartilageChemokinesJoint diseaseOsteoarthritis

Identifiers

PMID27856294
PMCPMC5430000
OpenAlexW2549862600

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.