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Anti‐apoptotic Bcl‐2 enhancing requires FGF‐2/FGF receptor 1 binding in mouse osteoblasts
Author(s) -
Agas Dimitrios,
Marchetti Luigi,
Menghi Giovanna,
Materazzi Stefano,
Materazzi Giovanni,
Capacchietti Mariolina,
Hurley Marja M.,
Sabbieti Maria Giovanna
Publication year - 2008
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.21170
Subject(s) - fibroblast growth factor receptor 1 , fibroblast growth factor , apoptosis , receptor , microbiology and biotechnology , chemistry , osteoblast , caspase , endocrinology , medicine , biology , programmed cell death , in vitro , biochemistry
In this study, we investigated the role of prostaglandin F2α (PGF2α) in mouse osteoblast survival and the function of fibroblast growth factor 2 (FGF‐2) and fibroblast growth factor receptor 1 (FGFR1) in this process. In particular, for the first time, we demonstrated that PGF2α increased osteoblast survival in a dose‐dependent manner and we showed that the effect is correlated with an increase in Bcl‐2/Bax ratio. Furthermore, we demonstrated that PGF2α caused a decrement of the active caspases 9 and 3. By blocking FGF‐2 with the specific neutralizing antibody and by depletion of FGFR1 gene with a specific siRNA, we showed that FGFR1 and FGF‐2 are critical for the increment of Bcl‐2/Bax ratio and the decrement of the active caspases 9 and 3, induced by PGF2α. Moreover, transmission electron microscopy studies showed that PGF2α increased binding of FGF‐2 and FGFR1 and co‐localization of reactive sites at plasma membrane level. In conclusion, we report a novel mechanism in which PGF2α induces FGF‐2 binding to its specific cell surface receptor 1 leading to a cascade pathway that culminates with increased mouse osteoblast survival. J. Cell. Physiol. 214:145–152, 2008. © 2007 Wiley‐Liss, Inc.