Intrafibrillar silicified collagen scaffold promotes in-situ bone regeneration by activating the monocyte p38 signaling pathway

Jin long Sun, Kai Jiao, Qun Song, Chu fan Ma, Chao Ma, Franklin Chi Meng Tay, Li na Niu, Ji hua Chen

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Intrafibrillar silicified collagen scaffold (SCS) is a promising biomaterial for bone regeneration because it promotes cell homing and angiogenesis in bone defects via monocyte modulation. In the present study, a rat femoral defect model was used to examine the contribution of monocyte signaling pathways to SCS modulation. Activation of the monocyte p38 signaling pathway by SCS resulted in monocyte differentiation into TRAP-positive mononuclear cells. These cells demonstrated increased secretion of SDF-1α VEGFa and PDGF-BB, which, in turn, promoted homing of bone marrow stromal cells (BMSCs) and endothelial progenitor cells (EPCs), as well as local vascularization. Monocyte differentiation and secretion were blocked after inhibition of the p38 pathway, which resulted in reduction in cell homing and angiogenesis. Taken together, these novel findings indicate that the p38 signaling pathway is crucial in SCS-modulated monocyte differentiation and secretion, which has a direct impact on SCS-induced bone regeneration. Statement of significance: Intrafibrillar silicified collagen scaffold (SCS) is a promising biomaterial for bone regeneration. The present work demonstrates that SCS possesses favorable bone regeneration potential in a rat femoral defect model. The degrading scaffold modulates monocyte differentiation and release of certain cytokines to recruit MSCs and EPCs, as well as enhances local vascularization by activating the p38 MAPK signaling pathway. These findings indicate that SCS contributes to bone defect regeneration by stimulating host cell homing and promoting local angiogenesis and osteogenesis without the need for loading cytokines or xenogenous stem cells.

Original languageEnglish (US)
Pages (from-to)354-365
Number of pages12
JournalActa biomaterialia
Volume67
DOIs
StatePublished - Feb 1 2018

Fingerprint

Bone Regeneration
Scaffolds (biology)
Collagen
Scaffolds
Monocytes
Bone
Defects
Endothelial cells
Biocompatible Materials
Thigh
Biomaterials
Rats
Modulation
Cytokines
p38 Mitogen-Activated Protein Kinases
Stem cells
Mesenchymal Stromal Cells
Osteogenesis
Stem Cells
Chemical activation

Keywords

  • Angiogenesis
  • Bone regeneration
  • Cell homing
  • Intrafibrillar silicification
  • Monocytes
  • p38 MAPK

ASJC Scopus subject areas

  • Biotechnology
  • Biomaterials
  • Biochemistry
  • Biomedical Engineering
  • Molecular Biology

Cite this

Intrafibrillar silicified collagen scaffold promotes in-situ bone regeneration by activating the monocyte p38 signaling pathway. / Sun, Jin long; Jiao, Kai; Song, Qun; Ma, Chu fan; Ma, Chao; Tay, Franklin Chi Meng; Niu, Li na; Chen, Ji hua.

In: Acta biomaterialia, Vol. 67, 01.02.2018, p. 354-365.

Research output: Contribution to journalArticle

Sun, Jin long ; Jiao, Kai ; Song, Qun ; Ma, Chu fan ; Ma, Chao ; Tay, Franklin Chi Meng ; Niu, Li na ; Chen, Ji hua. / Intrafibrillar silicified collagen scaffold promotes in-situ bone regeneration by activating the monocyte p38 signaling pathway. In: Acta biomaterialia. 2018 ; Vol. 67. pp. 354-365.
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abstract = "Intrafibrillar silicified collagen scaffold (SCS) is a promising biomaterial for bone regeneration because it promotes cell homing and angiogenesis in bone defects via monocyte modulation. In the present study, a rat femoral defect model was used to examine the contribution of monocyte signaling pathways to SCS modulation. Activation of the monocyte p38 signaling pathway by SCS resulted in monocyte differentiation into TRAP-positive mononuclear cells. These cells demonstrated increased secretion of SDF-1α VEGFa and PDGF-BB, which, in turn, promoted homing of bone marrow stromal cells (BMSCs) and endothelial progenitor cells (EPCs), as well as local vascularization. Monocyte differentiation and secretion were blocked after inhibition of the p38 pathway, which resulted in reduction in cell homing and angiogenesis. Taken together, these novel findings indicate that the p38 signaling pathway is crucial in SCS-modulated monocyte differentiation and secretion, which has a direct impact on SCS-induced bone regeneration. Statement of significance: Intrafibrillar silicified collagen scaffold (SCS) is a promising biomaterial for bone regeneration. The present work demonstrates that SCS possesses favorable bone regeneration potential in a rat femoral defect model. The degrading scaffold modulates monocyte differentiation and release of certain cytokines to recruit MSCs and EPCs, as well as enhances local vascularization by activating the p38 MAPK signaling pathway. These findings indicate that SCS contributes to bone defect regeneration by stimulating host cell homing and promoting local angiogenesis and osteogenesis without the need for loading cytokines or xenogenous stem cells.",
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AU - Tay, Franklin Chi Meng

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AU - Chen, Ji hua

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N2 - Intrafibrillar silicified collagen scaffold (SCS) is a promising biomaterial for bone regeneration because it promotes cell homing and angiogenesis in bone defects via monocyte modulation. In the present study, a rat femoral defect model was used to examine the contribution of monocyte signaling pathways to SCS modulation. Activation of the monocyte p38 signaling pathway by SCS resulted in monocyte differentiation into TRAP-positive mononuclear cells. These cells demonstrated increased secretion of SDF-1α VEGFa and PDGF-BB, which, in turn, promoted homing of bone marrow stromal cells (BMSCs) and endothelial progenitor cells (EPCs), as well as local vascularization. Monocyte differentiation and secretion were blocked after inhibition of the p38 pathway, which resulted in reduction in cell homing and angiogenesis. Taken together, these novel findings indicate that the p38 signaling pathway is crucial in SCS-modulated monocyte differentiation and secretion, which has a direct impact on SCS-induced bone regeneration. Statement of significance: Intrafibrillar silicified collagen scaffold (SCS) is a promising biomaterial for bone regeneration. The present work demonstrates that SCS possesses favorable bone regeneration potential in a rat femoral defect model. The degrading scaffold modulates monocyte differentiation and release of certain cytokines to recruit MSCs and EPCs, as well as enhances local vascularization by activating the p38 MAPK signaling pathway. These findings indicate that SCS contributes to bone defect regeneration by stimulating host cell homing and promoting local angiogenesis and osteogenesis without the need for loading cytokines or xenogenous stem cells.

AB - Intrafibrillar silicified collagen scaffold (SCS) is a promising biomaterial for bone regeneration because it promotes cell homing and angiogenesis in bone defects via monocyte modulation. In the present study, a rat femoral defect model was used to examine the contribution of monocyte signaling pathways to SCS modulation. Activation of the monocyte p38 signaling pathway by SCS resulted in monocyte differentiation into TRAP-positive mononuclear cells. These cells demonstrated increased secretion of SDF-1α VEGFa and PDGF-BB, which, in turn, promoted homing of bone marrow stromal cells (BMSCs) and endothelial progenitor cells (EPCs), as well as local vascularization. Monocyte differentiation and secretion were blocked after inhibition of the p38 pathway, which resulted in reduction in cell homing and angiogenesis. Taken together, these novel findings indicate that the p38 signaling pathway is crucial in SCS-modulated monocyte differentiation and secretion, which has a direct impact on SCS-induced bone regeneration. Statement of significance: Intrafibrillar silicified collagen scaffold (SCS) is a promising biomaterial for bone regeneration. The present work demonstrates that SCS possesses favorable bone regeneration potential in a rat femoral defect model. The degrading scaffold modulates monocyte differentiation and release of certain cytokines to recruit MSCs and EPCs, as well as enhances local vascularization by activating the p38 MAPK signaling pathway. These findings indicate that SCS contributes to bone defect regeneration by stimulating host cell homing and promoting local angiogenesis and osteogenesis without the need for loading cytokines or xenogenous stem cells.

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