Dexamethasone induces apoptosis of osteoblasts in culture by interference in cell adhesion complex

Abstract

Adhesive interactions play a critical role in cell biology, influencing vital processes from proliferation to cell death. The objective of this study was to analyse the effect of DEX (dexamethasone) on the biology of osteoblasts and its influence on the expression of ILK and β1 integrin. Primary human osteoblast culture were treated with dexamethasone in 10−9M (physiological) and 10−6M (pharmacological) doses of DEX for 24 and 48 hours. Cell viability (MTT assay), adhesion (crystal violet assay), apoptosis (flow cytometry), expression and immunolocalization of β1‐integrin and ILK (western blot and immunofluorescence) were analyzed. It was observed that cell viability and adhesion were reduced in the cultures evaluated. In comparison with the control cultures, there was slightly less apoptosis in the cultures exposed to the physiological dose and considerably more apoptosis in those exposed to the pharmacological dose. In all treated cultures, protein expression of ILK was slightly higher than in the control cultures, whereas that of β1 integrin was significantly lower. Both proteins under study were co‐localized at the cell periphery in all cultures. Our results suggest that DEX causes osteoblast anoikis, probably due to decreased β1 integrin expression, which might have had a direct influence upon ILK, reducing its activation and preventing it from playing its characteristic anti‐apoptotic role.Supported by FAPESP, CAPES