Evidence map›Paper›PMID 27612450›Full record

ArticleClinical and experimental immunology2016

Increased chemotaxis and activity of circulatory myeloid progenitor cells may contribute to enhanced osteoclastogenesis and bone loss in the C57BL/6 mouse model of collagen-induced arthritis.

M Ikić Matijašević, D Flegar, N Kovačić, V Katavić, T Kelava, A Šućur, S Ivčević, H Cvija, E Lazić Mosler, I Kalajzić and 2 more

Open access · greenAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-weighted citation impact, top 25% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. 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

12 authors at 3 institutions in 2 countries.

M Ikić MatijaševićDepartment of Physiology and Immunology, University of Zagreb School of Medicine, Zagreb, Croatia.
D FlegarDepartment of Physiology and Immunology, University of Zagreb School of Medicine, Zagreb, Croatia.
N KovačićLaboratory for Molecular Immunology, Croatian Institute for Brain Research, University of Zagreb School of Medicine, Zagreb, Croatia.
V KatavićLaboratory for Molecular Immunology, Croatian Institute for Brain Research, University of Zagreb School of Medicine, Zagreb, Croatia.
T KelavaDepartment of Physiology and Immunology, University of Zagreb School of Medicine, Zagreb, Croatia.
A ŠućurDepartment of Physiology and Immunology, University of Zagreb School of Medicine, Zagreb, Croatia.
S IvčevićDepartment of Physiology and Immunology, University of Zagreb School of Medicine, Zagreb, Croatia.
H CvijaDepartment of Physiology and Immunology, University of Zagreb School of Medicine, Zagreb, Croatia.
E Lazić MoslerLaboratory for Molecular Immunology, Croatian Institute for Brain Research, University of Zagreb School of Medicine, Zagreb, Croatia.
I KalajzićDepartment of Reconstructive Sciences, University of Connecticut Health Center, Farmington, CT, USA.
A MarušićDepartment of Research in Biomedicine and Health, University of Split School of Medicine, Split, Croatia.
D GrčevićDepartment of Physiology and Immunology, University of Zagreb School of Medicine, Zagreb, Croatia.ORCID http://orcid.org/0000-0002-2365-8249
University of Zagreb · HRUConn Health · USUniversity of Split · HR

Funding

Notch Signaling and Bone Fracture HealingR01AR055607 · NIAMS · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI Kurt David Hankenson, IVO Kalajzic · 2011 to 2026
$6.3M
NIAMS NIH HHS R01 AR055607
6 · The paper itself

Abstract

Our study aimed to determine the functional activity of different osteoclast progenitor (OCP) subpopulations and signals important for their migration to bone lesions, causing local and systemic bone resorption during the course of collagen-induced arthritis in C57BL/6 mice. Arthritis was induced with chicken type II collagen (CII), and assessed by clinical scoring and detection of anti-CII antibodies. We observed decreased trabecular bone volume of axial and appendicular skeleton by histomorphometry and micro-computed tomography as well as decreased bone formation and increased bone resorption rate in arthritic mice in vivo. In the affected joints, bone loss was accompanied with severe osteitis and bone marrow hypercellularity, coinciding with the areas of active osteoclasts and bone erosions. Flow cytometry analysis showed increased frequency of putative OCP cells (CD3

Indexed as

AnimalsArthritis, ExperimentalAutoantibodiesBiomarkersBiopsyBone Marrow CellsBone ResorptionCell DifferentiationChemotaxisCollagen Type IICytokinesDisease Models, AnimalImmunophenotypingMaleMiceMice, Inbred C57BLAutoantibodiesBiomarkersCollagen Type IICytokinesbone losschemokinescollagen-induced arthritisinflammationosteoclast progenitors

Identifiers

PMID27612450
PMCPMC5108074
OpenAlexW2518957594

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.