AbstractControl of osteoblast growth and development can be characterized from receptor mediated events to nuclear messengers controlling gene transcription. From this analysis it is possible to formulate a model to explain the reciprocal relationship between growth and differentiation as well as differential cytokine modulation of osteoblast function. Central to this model are putative tissue specific transcriptional switches (possibly of the bHLH gene superfamily) that may repress proliferation and permit the regulation of mature osteoblast phenotypic characteristics. This model proposes that in post‐mitotic differentiated osteoblasts, tissue specific transcription factors determine the capacity to express osteoblastic characteristic, whereas receptor activated signalling cascades, namely, cAMP/protein kinase A, receptor serine/threonine kinase, and vitamin D receptor‐dependent pathways, regulate mature osteoblast‐specific gene expression. Activated differentiation switches also may feedback to transcriptionally repress proliferation. Conversely, in preosteoblasts, in which differentiation switches are turned off, distinct signalling cascades involving tyrosine kinases, PKC, and
📖 افتح في inklap 🔗 DOI 📮 اطلب بحثاً