Bioactive Borate Glass Triggers Phenotypic Changes in Adipose Stem Cells


A bioactive borate glass, 13-93B3 (B3), has been used successfully in the clinic to treat chronic, nonhealing wounds without scarring. However, the mechanism by which B3 stimulates wound healing is poorly understood. Because adipose stem cells (ASCs) have been shown to have multiple roles in wound repair, we hypothesized that B3 triggers ASCs. In this study, we evaluate the effects of B3 on ASC survival, migration, differentiation, and protein secretion in vitro. In concentrations ≤10 mg/ml, B3 did not affect ASC viability under static conditions. B3 promoted the migration of ASCs but did not increase differentiation into bone or fat. B3 also decreased ASCs secretion of collagen I, PAI-1, MCP-1, DR6, DKK-1, angiogenin, IL-1, IGFBP-6, VEGF, and TIMP-2; increased expression of IL-1R and E-selectin; had a transient decrease in IL-6 secretion; and had a transient increase in bFGF secretion. Together, these results show that B3 alters the protein secretion of ASCs.


Materials Science and Engineering

Second Department

Biological Sciences

Keywords and Phrases

Glass; Proteins, Adipose stem cells; Borate glass; Collagen I; Phenotypic changes; Protein secretion; Static conditions; Wound healing; Wound repair, Stem cells, angiogenin; boric acid; collagen type 1; death receptor; death receptor 6; dickkopf 1 protein; endothelial leukocyte adhesion molecule 1; fat; glass; interleukin 1; interleukin 1 receptor; interleukin 6; monocyte chemotactic protein 1; plasminogen activator inhibitor; somatomedin binding protein 6; tissue inhibitor of metalloproteinase 2; unclassified drug; vasculotropin, adipose derived stem cell; adult; Article; cell differentiation; cell migration; cell survival; cell viability; DNA content; female; human; human cell; phenotype; priority journal; protein secretion; wound healing

International Standard Serial Number (ISSN)

0957-4530; 1573-4838

Document Type

Article - Journal

Document Version


File Type





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Publication Date

01 Apr 2020

PubMed ID