MCP/CCR2 Signaling Is Essential for Recruitment of Mesenchymal Progenitor Cells during the Early Phase of Fracture Healing

Ishikawa, Masahiro; Ito, Hiromu; Kitaori, Toshiyuki; Murata, Koichi; Shibuya, Hideyuki; Furu, Moritoshi; Yokota, Hiroyuki; Fujii, Takayuki; Yamamoto, Kōji; Matsuda, Shuichi

doi:10.1371/journal.pone.0104954

Cited by 70 publications

(67 citation statements)

References 41 publications

(45 reference statements)

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“…CCL2 is also thought to be a mediator of bone remodeling by recruiting monocytes/macrophages to the site of bone injury [38]. A recent study showed that CCL2-CCR2 signaling during the early phase of fracture healing is crucial for recruitment of mesenchymal progenitor cells [39]. Our results showed 7ND coating without PE particle infusion tended to decrease BMD compared to controls, while 7ND reversed PE particle-induced bone loss in PE particle infused group.…”

Section: Discussionmentioning

confidence: 47%

Mutant CCL2 protein coating mitigates wear particle-induced bone loss in a murine continuous polyethylene infusion model

et al. 2017

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Wear particle-induced osteolysis limits the long-term survivorship of total joint replacement (TJR). Monocyte/macrophages are the key cells of this adverse reaction. Monocyte Chemoattractant Protein-1 (MCP-1/CCL2) is the most important chemokine regulating trafficking of monocyte/macrophages in particle-induced inflammation. 7ND recombinant protein is a mutant of CCL2 that inhibits CCL2 signaling. We have recently developed a layer-by-layer (LBL) coating platform on implant surfaces that can release biologically active 7ND. In this study, we investigated the effect of 7ND on wear particle-induced bone loss using the murine continuous polyethylene (PE) particle infusion model with 7ND coating of a titanium rod as a local drug delivery device. PE particles were infused into hollow titanium rods with or without 7ND coating implanted in the distal femur for 4 weeks. Specific groups were also injected with RAW 264.7 as the reporter macrophages. Wear particle-induced bone loss and the effects of 7ND were evaluated by microCT, immunohistochemical staining, and bioluminescence imaging. Local delivery of 7ND using the LBL coating decreased systemic macrophage recruitment, the number of osteoclasts and wear particle-induced bone loss. The development of a novel orthopaedic implant coating with anti-CCL2 protein may be a promising strategy to mitigate peri-prosthetic osteolysis.

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Section: Discussionmentioning

confidence: 47%

Mutant CCL2 protein coating mitigates wear particle-induced bone loss in a murine continuous polyethylene infusion model

et al. 2017

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“…Depending upon the approach used, the output of analysis may vary (Kaas et al 2014). Therefore, a universal approach is needed to obtain consistent results.…”

Section: Discussionmentioning

confidence: 99%

Phylogenomic grouping of Listeria monocytogenes

et al. 2015

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The precise delineation of lineages and clonal groups are a prerequisite to examine within-species genetic variations, particularly with respect to pathogenic potential. A whole-genome-based approach was used to subtype and subgroup isolates of Listeria monocytogenes. Core-genome typing was performed, employing 3 different approaches: total core genes (CG), high-scoring segment pairs (HSPs), and average nucleotide identity (ANI). Examination of 113 L. monocytogenes genomes available in-house and in public domains revealed 33 phylogenomic groups (PGs). Each PG could be differentiated into a number of genomic types (GTs), depending on the approach used: HSPs (n = 57 GTs), CG (n = 71 GTs), and ANI (n = 83 GTs). Demarcation of the PGs was concordant with the 4 known lineages and led to the identification of sublineages in the lineage groups I, II, and III. In addition, PG assignments had discriminatory power similar to multi-virulence-locus sequence typing types and clonal complexes of multilocus sequence typing. Clustering of genomically highly similar isolates from different countries, sources, and isolation dates using whole-genome-based PG suggested that dispersion of phylogenomic clones of L. monocytogenes preceded their subsequent evolution. Classification according to PG may act as a guideline for future epidemiological studies.

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“…As one example, C‐C Motif Chemokine Ligand 2 (also known as Monocyte Chemoattractant Protein‐1) (CCL2 or MCP1) and its receptor Chemokine Receptor type 2 (CCR2) stimulate monocyte chemotaxis in the inflammatory response . CCL2 is expressed from days 1–3 in the fracture site . When subject to fracture, Ccl2 ‐null and Ccr2 ‐null mice both exhibit delayed fracture healing and decreased callus volume as a result of diminished mesenchymal cell infiltration and impaired vascularization …”

Section: Inflammatory Phase—inflammatory Cellsmentioning

confidence: 99%

Cellular biology of fracture healing

Bahney

Zondervan²,

Allison³

et al. 2018

Journal Orthopaedic Research

319

339

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The biology of bone healing is a rapidly developing science. Advances in transgenic and gene-targeted mice have enabled tissue and cell-specific investigations of skeletal regeneration. As an example, only recently has it been recognized that chondrocytes convert to osteoblasts during healing bone, and only several years prior, seminal publications reported definitively that the primary tissues contributing bone forming cells during regeneration were the periosteum and endosteum. While genetically modified animals offer incredible insights into the temporal and spatial importance of various gene products, the complexity and rapidity of healing— coupled with the heterogeneity of animal models—renders studies of regenerative biology challenging. Herein, cells that play a key role in bone healing will be reviewed and extracellular mediators regulating their behavior discussed. We will focus on recent studies that explore novel roles of inflammation in bone healing, and the origins and fates of various cells in the fracture environment.

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MCP/CCR2 Signaling Is Essential for Recruitment of Mesenchymal Progenitor Cells during the Early Phase of Fracture Healing

Cited by 70 publications

References 41 publications

Mutant CCL2 protein coating mitigates wear particle-induced bone loss in a murine continuous polyethylene infusion model

Mutant CCL2 protein coating mitigates wear particle-induced bone loss in a murine continuous polyethylene infusion model

Phylogenomic grouping of Listeria monocytogenes

Cellular biology of fracture healing

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