Abstract

Transforming Growth Factor beta1 (TGF beta1) exerts its functions both during embryogenesis, and in adult organism. TGF beta1 regulates cell proliferation, differentiation, motility and apoptosis. TGF beta1 is the most abundant growth factor in human bone. It is implicated in the pathogenesis of several bone diseases such as otosclerosis. During embryonic development, TGF beta1 plays a role in the migration of cells to the site of future skeletogenesis, the epithelial-mesenchymal interaction, and the formation of cellular condensations which dictates the general shape of the future skeletal elements. It also influences normal skeleton development by playing a critical role in inducing mesenchymal cell differentiation to either chondrocytes or osteoblasts. During Adult life, TGF beta1 has an influence on the maintenance of normal skeleton by playing a critical role on bone-forming cell namely, the osteoblast. TGF beta1 affects osteoblast differentiation, matrix formation, and mineralization. In MC3T3-E1 osteoblast-like cell line TGF beta1 inhibited the expression of the Runx2 and osteocalcin osteoblast differentiation markers. It interacts with many will known pathways in osteoblasts biology, such as Prostaglandin E2, Parathyroid hormone related peptide and Wnt-beta-catenin pathways. TGF beta1 exerts effects on osteocytes too. Treatment of pre-osteocytes with TGF alpha1 decreased cell death. Studied performed on osteoclast revealed that it inhibits both their proliferation and activity. This review briefly discusses the relation between this cytokine and the skeleton development and maintenance.

Keywords: Glycosaminoglycans - metabolism, Bone and Bones - metabolism, Bone Development - physiology, Osteoblasts - cytology, Signal Transduction, Transforming Growth Factor beta - metabolism, Transforming Growth Factor beta1