TGF‐β2 stimulates cranial suture closure through activation of the Erk‐MAPK pathway

Abstract

Cranial sutures are important growth sites of the skull. During suture closure, the dura mater is one of the most important sources of various positive and negative regulatory signals. Previous results indicate that TGF-beta2 from dura mater strongly accelerates suture closure, however, its exact regulatory mechanism is still unclear. In this study, we confirmed that removal of dura mater in calvarial organ culture strongly accelerates sagittal suture closure and that this effect is further enhanced by TGF-beta2 treatment. TGF-beta2 stimulated cell proliferation in the MC3T3-E1 cell line. Similarly, it stimulated the proliferation of cells in the sutural space in calvarial organ culture. Furthermore, TGF-beta2-mediated enhanced cell proliferation and suture closure were almost completely inhibited by an Erk-MAPK blocker, PD98059. These results indicate that TGF-beta2-induced activation of Erk-MAPK is an important signaling component that stimulates cell proliferation to enrich osteoprogenitor cells, thereby promoting their differentiation into osteoblasts to achieve a rapid calvarial bone expansion.

Growth factor TGF-β induces intestinal epithelial cell (IEC-6) differentiation: miR-146b as a regulatory component in the negative feedback loop

“…Importantly, ERK MAP kinase was also suggested to crosstalk with TGF-b signaling pathway components (Hayashida et al 2003;Lee et al 2006;Fujita et al 2004). Our data of immediate ERK1/2 signal activation in TGF-b stimulated IEC-6 cell differentiation are consistent with data acquired from other cell types.…”

Stem Cell Proliferation Pathways Comparison between Human Exfoliated Deciduous Teeth and Dental Pulp Stem Cells by Gene Expression Profile from Promising Dental Pulp

“…Our results showed that TGF-b2 and TGF-b3 were highly expressed in SHED compared with DPSCs. Because TGF-b2 has been reported to stimulate cell proliferation and collagen synthesis (26,27), it might regulate the biological activities of SHED. In addition, CTGF, whose expression was higher in SHED, is a matrix signaling molecule involved in TGF-b-induced cell proliferation, matrix synthesis, angiogenesis, migration, and osteoblast lineage differentiation of MSCs (28).…”

Gold nanoparticles with different charge and moiety induce differential cell response on mesenchymal stem cell osteogenesis

“…The up-regulation of FGF-2 could imply a dedifferentiation or a reversal of emphasis on cell proliferation rather than bone mineralization in differentiating hMSCs [36]. Moreover, an increase in TGF-b expression, in association with SMAD 3, could also hinder ALP activity and mineralization in osteoblasts [37] thereby promoting cell growth for a vast potential in many bone tissue regeneration strategies [38,39] (Fig. 7).…”