Abstract
Neural crest-derived (FOb) and mesoderm-derived (POb) calvarial osteoblasts are characterized by distinct differences in their osteogenic potential. We have previously demonstrated that enhanced activation of endogenous FGF and Wnt signaling confers greater osteogenic potential to FOb. Apoptosis, a key player in bone formation, is the main focus of this study. In the current work, we have investigated the apoptotic activity of FOb and POb cells during differentiation. We found that lower apoptosis, as measured by caspase-3 activity is a major feature of neural crest-derived osteoblast which also have higher osteogenic capacity. Further investigation indicated TGF-β signaling as main positive regulator of apoptosis in these two populations of calvarial osteoblasts, while BMP and canonical Wnt signaling negatively regulate the process. By either inducing or inhibiting these signaling pathways we could modulate apoptotic events and improve the osteogenic potential of POb. Taken together, our findings demonstrate that integration of multiple signaling pathways contribute to imparting greater osteogenic potential to FOb by decreasing apoptosis.
Highlights
Differences in the embryonic origin of mammalian bones composing the cranial vault have been established [1]
We have demonstrated that the neural crest derived-frontal osteoblasts (FOb) are endowed with enhanced activation of endogenous canonical Wnt signaling compared to the paraxial mesodermderived osteoblasts (POb) and that this signaling contributes to the greater osteogenic potential of frontal bone cells [2]
Apoptotic Activity Inversely Correlates with the Osteogenic Potential of FOb and POb
Summary
Differences in the embryonic origin of mammalian bones composing the cranial vault have been established [1]. Our initial work unveiled that the different embryonic origin of calvarial bones influences their osteogenic potential and tissue repair both in vitro and in vivo cells [2,3,4,5]. We have demonstrated that the neural crest derived-frontal osteoblasts (FOb) are endowed with enhanced activation of endogenous canonical Wnt signaling compared to the paraxial mesodermderived osteoblasts (POb) and that this signaling contributes to the greater osteogenic potential of frontal bone cells [2]. Evidence obtained from both in vitro and in vivo studies indicated that this differential signaling plays a critical role in conferring greater osteogenic potential and tissue regeneration to frontal bones [3,4,5]. Delineating regional differences in osteogenic potential based on embryonic origin and determining the role of differential signaling in imparting superior osteogenic potential and bone repair is an appealing challenge
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