الفهرس 
Aim of the studyOnly 14 pages are availabe for public view
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Abstract
INTRODUCTION
In human tissues, normal homeostasis requires balanced interactions between cells and a network of secreted proteins known as the extracellular matrix. These cooperative interactions involve numerous cytokines acting through specific cell-surface receptors. When the balance between the cells and the extracellular matrix is disturbed, disease can result. This is clearly evident in the interactions mediated by the cytokine transforming growth factor beta (TGF-β) (Blobe et al., 2000)
Transforming growth factors were discovered more than 20 years ago as secreted factors that induced the growth of non-transformed cells; since tumor cells, unlike normal cells, can usually grow in suspension, it was proposed that this transforming activity, secreted by tumor cells, plays a major role in the growth of tumors (DeLarco and Todaro, 1978; Sporn and Todaro, 1980). Then it has become apparent that most, if not all, cells produce TGF-β and that TGF-β inhibits the growth of a wide range of cells, particularly those of epithelial, endothelial, neuronal, and fibroblastic origins and those of the immune system.
Conversely, TGF-βs stimulate mesenchymal cells to proliferate and produce extracellular matrix and induce a fibrotic response in various tissues in vivo (McCartney-Francis et al., 1998, Massague, 1998, Gabbiani, 2003)
TGF-β has been identified that regulate a wide variety of biologi biological processes including cell growth, apoptosis, differentiation, migration, extracellular matrix (ECM) production, angiogenesis, immunity, and development (Sun and Davies, 1995).
TGF-β signaling also regulates the morphogenesis of many developing organs. The development of mouse tooth germ, which was a good model for organogenesis, provides a powerful tool for explaining the molecular mechanisms that control organogenesis. As ectodermal appendages, the tooth organ arises from complex and progressive interactions between an ectoderm, the oral epithelium and an underlying mesenchyme. Their morphogenesis was regulated by conserved signaling pathways, including TGF-β following tooth development (Huang and Chai, 2010).