Fabrication and biological properties of calcium phosphate/chitosan composite coating on titanium in modified SBF.

In order to increase the biocompatibility and bioactivity of chitosan, hydroxyapatite was in situ combined into the spin-coated chitosan layer on the titanium substrate by incubating in modified simulated body fluid (m-SBF). The calcium phosphate/chitosan (CaP/CS) composite prepared in m-SBF showed a homogeneous distribution of spherical nano-clusters. The hydrophilicity of the coatings was increased by performing NaOH post-treatment of CaP/CS composites, which also affected apatite formation. Biocompatibility of the coatings was assessed by investigating the cellular response of human osteoblast-like MG-63 cells with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Cell adhesion and osteogenic properties of the mesoporous CaP/CS composite were evaluated by SEM and ALPase assay, respectively. This in vitro study showed improved cell adhesion and differentiation on nanostructured CaP/CS composites. These results indicate that this CaP/CS composite could be a promising candidate for bone tissue engineering.

Functional roles of BCAR3 in the signaling pathways of insulin leading to DNA synthesis, membrane ruffling and GLUT4 translocation.

Breast cancer anti-estrogen resistance 3 (BCAR3) is an SH2-containing signal transducer and is implicated in tumorigenesis of breast cancer cells. In this study, we found that BCAR3 mediates the induction of ERK activation and DNA synthesis by insulin, but not by IGF-1. Specifically, the SH2 domain of BCAR3 is involved in insulin-stimulated DNA synthesis. Differential tyrosine-phosphorylated patterns of the BCAR3 immune complex were detected in insulin and IGF-1 signaling, suggesting that BCAR3 is a distinct target molecule of insulin and IGF-1 signaling. Moreover, microinjection of BCAR3 inhibitory materials inhibited membrane ruffling induced by insulin, while this did not affect insulin-mediated GLUT4 translocation. Taken together, these results demonstrated that BCAR3 plays an important role in the signaling pathways of insulin leading to cell cycle progression and cytoskeleton reorganization, but not GLUT4 translocation.