Biphasic silica/apatite co-mineralized collagen scaffolds stimulate osteogenesis and inhibit RANKL-mediated osteoclastogenesis

Kai Jiao, Li Na Niu, Qi Hong Li, Fa Ming Chen, Wei Zhao, Jun Jie Li, Ji Hua Chen, Christopher W Cutler, David Henry Pashley, Franklin Chi Meng Tay

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

The effects of a biphasic mineralized collagen scaffold (BCS) containing intrafibrillar silica and apatite on osteogenesis of mouse mesenchymal stem cells (mMSCs) and inhibition of receptor activator of nuclear factor κB ligand (RANKL)-mediated osteoclastogenesis were investigated in the present study. mMSCs were cultured by exposing to BCS for 7 days for cell proliferation/viability examination, and stimulated to differentiate in osteogenic medium for 7-21 days for evaluation of alkaline phosphatase activity, secretion of osteogenic deposits and expression of osteoblast lineage-specific phenotypic markers. The effect of BCS-conditioned mMSCs on osteoclastogenesis of RAW 264.7 cells was evaluated by tartrate-resistant acid phosphatase staining and resorption pit analysis. The contributions of mitogen-activated protein kinase (MAPK) and phosphatidylinositol-3 kinase (PI3K) signal transduction pathways to osteogenesis of mMSCs and their osteoprotegerin (OPG) and RANKL expressions were also evaluated. Compared with unmineralized, intrafibrillarly-silicified or intrafibrillarly-calcified collagen scaffolds, BCS enhanced osteogenic differentiation of mMSCs by activation of the extracellular signal regulated kinases (ERK)/MAPK and p38/MAPK signaling pathways. After mMSCs were exposed to BCS, they up-regulated OPG expression and down-regulated RANKL expression through activation of the p38/MAPK and PI3K/protein kinase B (Akt) pathways, resulting in inhibition of the differentiation of RAW 264.7 cells into multinucleated osteoclasts and reduction in osteoclast function. These observations collectively suggest that BCS has the potential to be used in bone tissue engineering when the demand for anabolic activities is higher than catabolic metabolism during the initial stage of wound rehabilitation.

Original languageEnglish (US)
Pages (from-to)23-32
Number of pages10
JournalActa biomaterialia
Volume19
DOIs
StatePublished - Jun 1 2015

Fingerprint

Apatites
Apatite
Scaffolds (biology)
Collagen
Osteogenesis
Scaffolds
Silicon Dioxide
Stem cells
Mesenchymal Stromal Cells
Silica
Proteins
p38 Mitogen-Activated Protein Kinases
Phosphatidylinositol 3-Kinase
Osteoprotegerin
Phosphatases
Osteoclasts
Chemical activation
Signal transduction
Proto-Oncogene Proteins c-akt
Osteoblasts

Keywords

  • Hydroxyapatite
  • Intrafibrillar mineralization
  • Osteoclastogenesis
  • Osteogenesis
  • Osteoprotegerin

ASJC Scopus subject areas

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

Cite this

Biphasic silica/apatite co-mineralized collagen scaffolds stimulate osteogenesis and inhibit RANKL-mediated osteoclastogenesis. / Jiao, Kai; Niu, Li Na; Li, Qi Hong; Chen, Fa Ming; Zhao, Wei; Li, Jun Jie; Chen, Ji Hua; Cutler, Christopher W; Pashley, David Henry; Tay, Franklin Chi Meng.

In: Acta biomaterialia, Vol. 19, 01.06.2015, p. 23-32.

Research output: Contribution to journalArticle

Jiao, Kai ; Niu, Li Na ; Li, Qi Hong ; Chen, Fa Ming ; Zhao, Wei ; Li, Jun Jie ; Chen, Ji Hua ; Cutler, Christopher W ; Pashley, David Henry ; Tay, Franklin Chi Meng. / Biphasic silica/apatite co-mineralized collagen scaffolds stimulate osteogenesis and inhibit RANKL-mediated osteoclastogenesis. In: Acta biomaterialia. 2015 ; Vol. 19. pp. 23-32.
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AU - Chen, Fa Ming

AU - Zhao, Wei

AU - Li, Jun Jie

AU - Chen, Ji Hua

AU - Cutler, Christopher W

AU - Pashley, David Henry

AU - Tay, Franklin Chi Meng

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KW - Hydroxyapatite

KW - Intrafibrillar mineralization

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KW - Osteogenesis

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