Overexpression of Dlx5 in Chicken Calvarial Cells Accelerates Osteoblastic Differentiation

BMP-2-induced Runx2 Expression Is Mediated by Dlx5, and TGF-β1 Opposes the BMP-2-induced Osteoblast Differentiation by Suppression of Dlx5 Expression

“…It is highly correlated with previous reports that showed the role of Dlx5 is developmentally highly conserved in skeletal tissue development (19,20) and osteoblast differentiation (14,17,18). In addition, Dlx5 expression was specifically induced by stimulation of the BMP signaling pathway, such as direct application of BMP-2 or BMP-4 ligands, overexpression of constitutively active BMPR-I receptors, and overexpression of BMP-regulated Smads.…”

“…Reverse transcription was performed with a Superscript TM firststrand synthesis system for RT-PCR. 1 g of total cellular RNA as a template, 0.5 g of oligo(dT) [12][13][14][15][16][17][18] , 200 units of Superscript II reverse transcriptase, 0.1 volume of 10ϫ reverse transcription buffer, 0.5 mM of dNTP mixture (each of dATP, dCTP, dGTP, and dTTP), 10 mM of dithiothreitol were used for first strand cDNA synthesis for 60 min at 42°C. To eliminate contamination by RNA, the reverse-transcribed cDNA mixture was incubated with 2 units of RNase H for 20 min at 37°C.…”

“…Forced expression of Dlx5 leads to osteocalcin expression and a fully mineralized matrix in cell culture (14,18). Normally, Dlx5 expression is detected in discrete neuronal tissues and developing skeletal elements such as cartilage, bone, and tooth (19,20).…”

TGFβ-mediated FGF signaling is crucial for regulating cranial neural crest cell proliferation during frontal bone development

“…Loss of Dlx5 results in multiple craniofacial defects including agenesis of frontal bones (Depew et al, 1999;Tadic et al, 2002;Holleville et al, 2003). The similarity in frontal bone development defect between the Tgfbr2 fl/fl ;Wnt1-Cre and Dlx5 mutant mice suggests that TGF␤ and DLX signaling network may function together to regulate osteoblast differentiation during calvarial morphogenesis.…”

Dlx genes and the maintenance of bone homeostasis and skeletal integrity

“…RNA-Seq analysis of Dlx3 OCN-cKO metaphysis shows upregulation of transcription factors essential for osteoblastogenesis, including Runx2, 16 its downstream osteoblast-specific target Sp7 17 and Dlx5/Dlx6, two positive regulators of chondrocyte and osteoblast differentiation (see Figure 1). 8,9,18,19 The fact that Dlx3 plays an important role in regulating osteoblast activity is further supported by the analysis of Dlx3-deleted bone marrow stroma cells (BMSCs), which also shows increased osteoblast differentiation and bone-forming activity associated with increased gene expression of Runx2 and Dlx5. The notion that DLX3 acts as a negative regulator of osteoblastogenesis by reducing Runx2, Sp7, Dlx5 and Dlx6 gene expression is further supported by ChIP analysis on BMSCs, which shows that DLX3 binds to the promoters of Sp7, Dlx5 and Dlx6 and Runx2, directly modulating their activity (see also Hassan et al 12 ).…”