The effect of S53P4-based borosilicate glasses and glass dissolution products on the osteogenic commitment of human adipose stem cells

S53P4基硼硅酸盐玻璃及玻璃溶解产物对人类脂肪干细胞成骨作用的影响

阅读:9
作者:Miina Ojansivu, Ayush Mishra, Sari Vanhatupa, Miia Juntunen, Antonina Larionova, Jonathan Massera, Susanna Miettinen

Abstract

Despite the good performance of silicate bioactive glasses in bone regeneration, there is considerable potential to enhance their properties by chemical modifications. In this study, S53P4-based borosilicate glasses were synthesized and their dissolution profile was studied in simulated body fluid by assessing pH change, ion release and conversion to hydroxyapatite. The viability, proliferation, attachment, osteogenesis and endothelial marker expression of human adipose stem cells (hASCs) was evaluated upon direct culture on glass discs and in the extract medium. This is the first study evaluating cell behavior in response to borosilicate glasses based on S53P4 (commercially available as BonAlive®). Replacing silicate with borate in S53P4 increased the glass reactivity. Despite the good viability of hASCs under all conditions, direct culture of cells on borosilicate discs and in undiluted extract medium reduced cell proliferation. This was accompanied with changes in cell morphology. Regarding osteogenic commitment, alkaline phosphatase activity was significantly reduced by the borosilicate glass discs and extracts, whereas the expression of osteogenic markers RUNX2a, OSTERIX, DLX5 and OSTEOPONTIN was upregulated. There was also a borosilicate glass-induced increase in osteocalcin protein production. Moreover, osteogenic supplements containing borosilicate extracts significantly increased the mineral production in comparison to the osteogenic medium control. Interestingly, borosilicate glasses stimulated the expression of endothelial markers vWF and PECAM-1. To conclude, our results reveal that despite reducing hASC proliferation, S53P4-based borosilicate glasses and their dissolution products stimulate osteogenic commitment and upregulate endothelial markers, thus supporting their further evaluation for regenerative medicine.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。