By Bernard V. Perbal (Editor), Masaharu Takigawa (Editor)
CCN Protein: a brand new family members of mobile progress and Differentiation Regulators provides the latest development within the box of CCN proteins, a brand new kinfolk of secretory signaling molecules which are fascinated by a number of primary organic growth. those proteins percentage a different multimodular association and current a partial id with 4 households of regulatory proteins controling progress and improvement. The e-book covers the jobs of CCN proteins within the keep watch over of mobile proliferation and differentiation in the course of general improvement, wound fix, chondrogenesis and bone improvement, angiogenesis, tissue regeneration, fibrosis, renal illnesses and melanoma improvement.
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Extra resources for CCN Proteins: A New Family of Cell Growth and Differentiation Regulators
Sample text
2001)] 23 24 Takigawa M, Nishida T & Kubota S Table 1. , 2003) Typical cells, tissues, and organs that express CCN2 are listed. + + +: strong, ++: moderate, +: weak. , 2005). Even in 3-week-old mice, hypertrophic chondrocytes in the growth plate of long bones expressed CCN2 (Oka M and Takigawa M, unpublished). , 2003) (Table 1). , 2003). These findings agree with the results showing that its in vivo expression was predominant in hypertrophic chondrocytes in growth plate cartilage, suggesting an autocrine/paracrine action of CCN2.
2005). Even in 3-week-old mice, hypertrophic chondrocytes in the growth plate of long bones expressed CCN2 (Oka M and Takigawa M, unpublished). , 2003) (Table 1). , 2003). These findings agree with the results showing that its in vivo expression was predominant in hypertrophic chondrocytes in growth plate cartilage, suggesting an autocrine/paracrine action of CCN2. , 2000). , 2000). It also increased the proteoglycan synthesis and gene expressions of aggrecan and collagen type II, typical markers of chondrocyte maturation, in both types of cells in confluent cultures in which they were maturing.
At the early healing stage after tooth extraction, CCN2 was expressed strongly in the residual periodontal ligament and in the endothelial cells and undifferentiated fibroblast-like cells, possibly mesenchymal stem cells, migrating into the granulation tissue at the bottom of the sockets (Table 1). At a later stage, osteoblast-like cells proliferated in the sockets, which showed low CCN2 expression. These findings suggest that CCN2 produced by residual periodontal cells, endothelial cells and undifferentiated mesenchymal cells, acts as an autocrine/paracrine factor in the sockets, causing the mesenchymal cells to differentiate into osteoblasts or the recruitment of osteoblasts from bone, which then replace the granulation tissue with bone.