B2A, a receptor modulator, increases the growth of pluripotent and preosteoblast cells through bone morphogenetic protein receptors.
Growth Factors
; 30(6): 410-7, 2012 Dec.
Article
em En
| MEDLINE
| ID: mdl-23231667
ABSTRACT
B2A (B2A2-K-NS) is a synthetic, multidomain peptide which is being developed to augment spinal fusion and bone repair locally. Using pluripotent mesenchymal cells of murine and human origin, we show that B2A-induced cell proliferation in a modest but dose-dependent manner. However, essentially all human tumor lines tested were not responsive or were weakly responsive to B2A. B2A treatment activated extracellular signal-regulated kinases 1 and 2 (ERK1/2), and the proliferation was partially blocked by an mitogen-activated protein kinase (MEK) inhibitor. The bone morphogenetic protein (BMP) type I receptor kinase inhibitors depressed B2A-induced proliferation. Upregulation of bone morphogenetic protein 2 was not involved, as noggin, DAN, or chordin did not block B2A-induced proliferation. These data suggest that B2A-induced proliferation results from cell-type-specific activation of bone morphogenetic protein receptor, which, in turn, regulates ERK1/2 activity. B2A-induced proliferation, acting through ERK1/2, is a phenomenon that, while not strictly related to the ability of B2A to augment BMP-induced differentiation via the small mothers against decapentaplegic pathway, may ultimately contribute to bone repair in vivo.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Osteoblastos
/
Peptídeos
/
Receptores de Proteínas Morfogenéticas Ósseas
Limite:
Animals
/
Humans
Idioma:
En
Revista:
Growth Factors
Assunto da revista:
BIOLOGIA
Ano de publicação:
2012
Tipo de documento:
Article
País de afiliação:
Estados Unidos