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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Effect of dexamethasone on human osteoblasts in culture: involvement of beta 1 integrin and integrin-linked kinase

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Author(s):
Naves, Marcelo A. [1] ; Pereira, Rosa M. R. [2] ; Comodo, Andreia N. [1] ; de Alvarenga, Erika L. F. C. [1] ; Caparbo, Valeria F. [2] ; Teixeira, Vicente P. C. [3, 1]
Total Authors: 6
Affiliation:
[1] Univ Fed Sao Paulo, Dept Pathol, Sao Paulo - Brazil
[2] Univ Sao Paulo, Sch Med, Div Rheumatol, Sao Paulo - Brazil
[3] Univ Fed Sao Paulo, Dept Internal Med, Div Nephrol, Sao Paulo - Brazil
Total Affiliations: 3
Document type: Journal article
Source: Cell Biology International; v. 35, n. 11, p. 1147-1151, NOV 2011.
Web of Science Citations: 9
Abstract

Adhesive interactions play a critical role in cell biology, influencing vital processes from proliferation to cell death. Integrins regulate cell-ECM (extracellular matrix) adhesion and must associate with phosphorylating proteins such as ILK (integrin-linked kinase). Dysregulation of ILK expression is associated with anchorage-independent growth, cell survival and inhibition of apoptosis. Glucocorticoids influence differentiation and adhesion of osteoblasts and can affect bone protein synthesis. The objective of this study was to analyse the effect of DEX (dexamethasone) on the biology of osteoblasts, together with its influence on the expression of ILK and beta 1 integrin. For this, primary cultures of human osteoblasts were exposed to DEX at 10(-9) M (physiological dose) and 10(-6) M (pharmacological dose) for 24 and 48 h. Cell viability, apoptosis and cell adhesion were analysed, as well as protein expression of beta 1 integrin and ILK. 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 beta 1 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 beta 1 integrin expression, which might have had a direct influence upon ILK, reducing its activation and preventing it from playing its characteristic antiapoptotic role. (AU)