THE ROLE OF LIPID PHOSPHATASE SHIP IN SKELETAL DEVELOPMENT
Mauricio Isaac1, Olin Liang2.
1Santa Barbara City College, Santa Barbara, CA, 2Brown University, Providence, RI.
Much of the mammalian skeleton originates from cartilage templates through endochondral ossification. The transition from cartilage is tightly coupled with chondrocyte proliferation, hypertrophy, blood vessel invasion, and osteoblast differentiation. A corollary of the complexity in skeletal development is a high incidence and wide range of the osteochondrodysplasia at an early age which frequently constitutes high risk for skeleton degenerative diseases in the adult. Our long-term goal is to elucidate the mechanisms that regulate endochondral bone development, a critical discovery for novel treatments of human skeletal diseases and injuries. Despite the fact that many of the growth factors important to cartilage development and functions are able to activate the phosphatidylinositol 3-kinase (PI3K) signaling transduction pathway, little is known about the role of PI3K signaling in osteochindral progenitor cell biology and its contribution to the mammalian skeletogenesis. The SH2-containing inositol 5’phosphatase 1 (SHIP) modulates P13K-initiated signaling by limiting membrane recruitment and activation of its downstream effector AKT. Here, based on our preliminary data, we hypothesize that SHIP plays a key role in the structural formation of vertebrate skeleton.