Combination of in silico and cell culture strategies to predict biomaterial performance: Effects of sintering temperature on the biological properties of hydroxyapatite.

Advances in methodologies to evaluate biomaterials brought an explosive growth of data, ensuing computational challenges to better analyzing them and allowing for high-throughput profiling of biological systems cost-efficiently. In this sense, we have applied bioinformatics tools to better understand the biological effect of different sintering temperatures of hydroxyapatite (abbreviated HA; at 1100, 1150, and 1250°C) on osteoblast performance. To do, we have better analyzed an earlier deposited study, in which the access code is E-MTAB-7219, which the authors have explored different in silico tools on this purpose.

Epigenetic Differences Arise in Endothelial Cells Responding to Cobalt-Chromium.

Cobalt-chromium (Co-Cr)-based alloys are emerging with important characteristics for use in dentistry, but the knowledge of epigenetic mechanisms in endothelial cells has barely been achieved. In order to address this issue, we have prepared a previously Co-Cr-enriched medium to further treat endothelial cells (HUVEC) for up to 72 h. Our data show there is important involvement with epigenetic machinery.

Bioactivity of the Protein Hydrolysates Obtained from the Most Abundant Crustacean Bycatch.

The animals from bycatch of the shrimp fisheries can be a source of natural products and bioactive compounds. Thus, the present study aimed to evaluate the bioactivity of protein hydrolysates prepared from the two most abundant crabs from the bycatch of shrimp fisheries in Brazil (Callinectes ornatus and Hepatus pudibundus). Samples of C.

The molecular pathway triggered by zirconia in endothelial cells involves epigenetic control.

The requirement to achieve natural looking restorations is one of the most challenging aspects in dentistry. Although zirconia has provided new opportunities for achieving superior aesthetics and physicochemical outcomes, very little has been achieved for its cellular and molecular performance, especially considering angiogenesis and osteogenesis. As angiogenesis is a secondary event and concomitant to osteogenesis, an indirect effect of dental implant on endothelial cells could be the release of active molecules such as those already reported affecting osteoblasts.

Osteogenic gene markers are epigenetically reprogrammed during contractile-to-calcifying vascular smooth muscle cell phenotype transition.

The understanding of vascular calcification-based mechanism is an urgent pending task in vascular biology and this prompted us to better address this issue by investigating whether DNA methylation mechanism might drive osteogenic marker genes modulation in primary human vascular smooth muscle cells (VSMCs) responding to calcium and phosphate levels overload up to 72 h. Firstly, our data shows this calcifying process recapitulates the molecular repertory of osteogenic biomarkers and specifically requiring RUNX2, Osterix and ALP, BSP genes activations along 72 h in vitro, and this behavior was validated here using other lineages. Conversely, both BMPs 4 and 7 were significantly overexpressed, maybe already as a mechanism in response to RUNX2 and Osterix genes activities identified earlier in response to the calcifying condition, and taken into maintain the calcifying phenotype of VSMCs.

HOXA cluster gene expression during osteoblast differentiation involves epigenetic control.

The HOXA gene cluster is generally recognized as a pivotal mediator of positional identity in the skeletal system, expression of different orthologues conferring alternative locational phenotype of the vertebrate bone. Strikingly, however, the molecular mechanisms that regulate orthologue-specific expression of different HOXA cluster members in gestating osteoblasts remain largely obscure, but in analogy to the processes observed in acute lymphatic leukemia it is assumed that alternative methylation of HOXA promoter regions drives position specific expression patterns. In an effort to understand HOXA cluster gene expression in osteogenesis we characterize both expression and the epigenetic landscape of the HOXA gene cluster during in vitro osteoblast formation from mesenchymal precursors.