Mouse pre-osteoblastic MC3T3-E1 cell adhesion, spreading, proliferation, mineralization, and expression of integrin subunits of α1, α2, β1, and gene markers of osteocalcin, osteopontin, alkaline phosphatase (ALP), and collagen type I were investigated on these two series of honeycomb films and their flat control.
Osteogenic differentiation of hASCs on SF-PET and PET constructs was also observed by extracellular matrix mineralization and expression of osteogenic-related markers (osteocalcin, osteopontin and collagen type I) after 28 days of osteogenic culture, in comparison to the control basal medium.
Indeed, calvarial cells derived compound heterozygous Pkd1+/Δ Kif3a+/Δ mice had alkaline phosphatase activity, mineralization and expression of Runx2 and osteocalcin transcripts that did not differ from wild-type control cultures (Fig. 3C 3F).
For example, activation of β-catenin in mature cartilage cells stimulates hypertrophy, matrix mineralization, and expression of VEGF, ADAMTS5, MMP-13, and several other MMPs [ 184].
Outcome measures included alkaline phosphatase expression, matrix mineralization, and expression of osteogenic genes (alkaline phosphatase, osteocalcin and bone morphogenetic protein receptor-1A) as measured by quantitative PCR.
The activation of WNT/β-catenin WNT/β-catenintnatal growth plate chondrocytes stinulates hypertrophy, mature mineralization, and expostnatalof VEgrowthAMTS5, MMplate and several other MMPs [ 183].
Their osteogenic effect was evaluated by using validated models including alkaline phosphatase (ALP) assay, mineralization assay and expression of osteogenic genes-bone morphogenetic protein-2 (BMP-2) and osteoblast transcription factor (RUNX2) – in primary calvarial cultures harvested from neonatal mice.
The honeycomb films, especially those with smaller pores, could significantly promote MC3T3-E1 cell adhesion, spreading, proliferation, ALP activity, mineralization, and gene expression of osteoblastic markers, via fostering expression of integrin subunits.
Activator-treated SCAPs exhibited an enhanced ALP activity, increased calcium deposition, and upregulated expression of odonto/osteogenic genes and proteins, while inhibitor-treated cells presented the lower ALP activity, decreased mineralization, and downregulated expression of odonto/osteoblast markers.
The results indicated that treatment of 0.1 to 10 μM Rb2 promoted the proliferation of MC3T3-E1 cells, improved alkaline phosphatase (ALP) expression, elevated calcium mineralization and mRNA expressions of Alp, Col1a1, osteocalcin (Ocn) and osteopontin (Opn) against oxidative damage induced by H2O2.
Mineralization and osteocalcin expression was demonstrated by (immuno)histochemistry.
