Graduate Student Directory
|Degree Program:||Molecular, Cellular, and Developmental Biology||Email:||firstname.lastname@example.org|
Our lab generated COX-2 transgenic mice for investigating the functional roles of COX-2 in embryo development, physiological and pathophysiological conditions. These COX-2 transgenic mice have been shown various developmental defects such as umbilical hernia, failure of eye formation and especially malformation of appendicular skeletons (long bones) with minor defect in skull (flat bones). In contrast to flat bone formation, the long bones are generated through the differentiation from mesenchyme to chondrocytes and following replacement with bone cells. Because of this reason, we are interested in the functional role of COX-2 in long bone formation, especially in chondrocyte differentiation. There have been several controversial researches have been shown that prostaglandin E2, which is one of downstream product of COX-2, inhibits chondrocyte differentiation and also stimulates bone formation and bone resorption. Of course the role of COX-2 in normal chondrocyte development, we are also interested in pathological function of COX-2 in articular cartilage, osteoarthritis (OA). OA is the most prevalent degenerative joint disease. In OA patients, the COX-2 expression is highly increased and its expression pattern is correlated with progression of OA. Recently, induction of selective COX-2 inhibition is emerging as a new target of cure of OA. Therefore, we are expecting that COX-2 transgenic and null mice can be used for unveiling the secret of COX-2 role in bone formation and OA.