SOX9, a transcription factor of the sex determining re gion Y related high mobility group box family of proteins, is crucial for skeletal development and marks all osteoblastic progenitors, being capable of indu cing RUNX2 expression. However, the role of SOX9 in osteoblastic differentiation is not completely understood. figure 1 Conditional deletion of SOX9 in the limb bud mesenchyme led to the absence of chondrocytes and osteo blasts. Contrastingly, when SOX9 was deleted in the neural crest cells that contribute to the craniofacial skel eton, the cells which normally Inhibitors,Modulators,Libraries form chondrocytes expressed osteoblasts markers, suggesting the existence of a the bipotential progenitor. However, SOX9 is not expressed by mature osteoblasts and this is the probable cause of its downregulation after 2 h of the stimulus.

COL1 and COL4A display functions related with the building of the basal membrane for the newly formed mature bone Inhibitors,Modulators,Libraries tissue. A recent report of comparative transcription of various fetal and adult mesenchymal stem cells sources through quantitative PCR profiling un veiled that collagens, such as collagen 1 and 4, were upregulated during several types of osteogenic differenti ation, such as the one reported in this manuscript with the levels of these two extracellular matrix components being increased. Supporting these findings, it has been reported that site mutations in collagen 1 leads to high bone mass in osteogenesis imperfecta. Since the bHLH transcription factor Twist inhibits osteoblast differentiation through binding to a DNA binding domain Anacetrapib in RUNX2, the early downregulation Inhibitors,Modulators,Libraries of this gene to levels below the basal level at 10 and 30 min could be indicative that the differentiation process was mediated by RUNX2.

Moreover, it has Inhibitors,Modulators,Libraries been shown that RUNX2, a Runt domain containing transcription fac tor, is indispensable for osteoblastic differentiation during both endochondral and intramembranous ossification and the function of mature osteoblasts, including the synthesis of bone matrix. Homozygous deletion of Runx2 in mice resulted in a complete lack of osteoblasts. Our results show a sustained selleckchem increase in the mRNA levels of this tran scription factor after 30 min, pointining to the involve ment of this gene in the osteogenesis induced by exposure to BMP2. Another essential gene related with osteoblastic differentiation is OSX, a transcription factor containing three zinc fingers. OSX was discovered as a BMP induced gene in C2C12 cells, with its deletion resulting in complete absence of osteoblasts in mouse embryos, despite the relatively normal expression of RUNX2, which indicates that OSX is activated after RUNX2 during osteoblastic differentiation.