Evidence map›Paper›PMID 25133509›Full record

ArticlePloS one2014

MCP/CCR2 signaling is essential for recruitment of mesenchymal progenitor cells during the early phase of fracture healing.

Masahiro Ishikawa, Hiromu Ito, Toshiyuki Kitaori, Koichi Murata, Hideyuki Shibuya, Moritoshi Furu, Hiroyuki Yoshitomi, Takayuki Fujii, Koji Yamamoto, Shuichi Matsuda

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

45 citing papers in PubMed, 83 citations in OpenAlex.

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  10. Increased neutrophil extracellular traps caused by diet-induced obesity delay fracture healing.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
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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

10 authors at 1 institution in 1 country.

Masahiro IshikawaDepartment of Orthopaedic Surgery, Kyoto University Graduate School of Medicine, Kyoto, Japan; Department of the Control for Rheumatic Disease, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Hiromu ItoDepartment of Orthopaedic Surgery, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Toshiyuki KitaoriDepartment of Orthopaedic Surgery, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Koichi MurataDepartment of Orthopaedic Surgery, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Hideyuki ShibuyaDepartment of Orthopaedic Surgery, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Moritoshi FuruDepartment of Orthopaedic Surgery, Kyoto University Graduate School of Medicine, Kyoto, Japan; Department of the Control for Rheumatic Disease, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Hiroyuki YoshitomiThe Center for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Takayuki FujiiDepartment of Orthopaedic Surgery, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Koji YamamotoCenter for the Promotion of Interdisciplinary Education and Research, Kyoto University, Kyoto, Japan.
Shuichi MatsudaDepartment of Orthopaedic Surgery, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Kyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThe purpose of this study was to investigate chemokine profiles and their functional roles in the early phase of fracture healing in mouse models.

methodsThe expression profiles of chemokines were examined during fracture healing in wild-type (WT) mice using a polymerase chain reaction array and histological staining. The functional effect of monocyte chemotactic protein-1 (MCP-1) on primary mouse bone marrow stromal cells (mBMSCs) was evaluated using an in vitro migration assay. MCP-1-/- and C-C chemokine receptor 2 (CCR2)-/- mice were fractured and evaluated by histological staining and micro-computed tomography (micro-CT). RS102895, an antagonist of CCR2, was continuously administered in WT mice before or after rib fracture and evaluated by histological staining and micro-CT. Bone graft exchange models were created in WT and MCP-1-/- mice and were evaluated by histological staining and micro-CT.

resultsMCP-1 and MCP-3 expression in the early phase of fracture healing were up-regulated, and high levels of MCP-1 and MCP-3 protein expression observed in the periosteum and endosteum in the same period. MCP-1, but not MCP-3, increased migration of mBMSCs in a dose-dependent manner. Fracture healing in MCP-1-/- and CCR2-/- mice was delayed compared with WT mice on day 21. Administration of RS102895 in the early, but not in the late phase, caused delayed fracture healing. Transplantation of WT-derived graft into host MCP-1-/- mice significantly increased new bone formation in the bone graft exchange models. Furthermore, marked induction of MCP-1 expression in the periosteum and endosteum was observed around the WT-derived graft in the host MCP-1-/- mouse. Conversely, transplantation of MCP-1-/- mouse-derived grafts into host WT mice markedly decreased new bone formation.

conclusionsMCP-1/CCR2 signaling in the periosteum and endosteum is essential for the recruitment of mesenchymal progenitor cells in the early phase of fracture healing.

Indexed as

AnimalsCells, CulturedChemokine CCL2Fracture HealingMesenchymal Stem CellsMiceMice, KnockoutReal-Time Polymerase Chain ReactionReceptors, CCR2Signal TransductionCcr2 protein, mouseChemokine CCL2Receptors, CCR2

Identifiers

PMID25133509
PMCPMC4136826
OpenAlexW1982753152

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.