Dimitrios Agas

TL;DR: It is strongly demonstrated that endogenous FGF‐2 is important in the maximal responses of BMP‐2 in bone and that this may be dependent on the p42/44 MAPK signaling pathway and downstream modulation of Runx2.

TL;DR: Investigation of the effect of haplo-insuffiency on bone loss in vertebrae from Fgf2+/- mutant mice found reduced bone nodule formation may correlate with impaired FGFR signaling, decreased Runx2 gene expression.

TL;DR: The results suggest that endogenous FGF‐2 is important in PTH effects on osteoblast proliferation, differentiation, and apoptosis, and reduced expression of these factors may contribute to the reduced anabolic response to PTH in the Fgf2−/− mice.

TL;DR: It is concluded that the impaired nuclear accumulation of Runx‐2 in Fgf2−/− osteoblasts reduces R‐Smads sub‐nuclear targeting with a consequent decreased expression of differentiating markers and impaired bone formation in F gf2 null mice.

TL;DR: It is demonstrated that phthalates induce osteoblast apoptosis, which is, at least in part, mediated by p53 activation, suggesting that the proliferative effects could be due to p53 missing activation or p53 mutation.