Dr. Julia Oxford
Dexamethasone, a corticosteroid that inhibits inflammation, is commonly used for the treatment of arthritis. However, glucocorticoid-induced osteoporosis is a side effect that commonly occurs after dexamethasone treatment. One of the mechanisms by which glucocorticoids are thought to suppress bone formation is through their effect on the wnt/ ß-catenin signaling pathway. The wnt/ ß-catenin pathway is essential in the formation of new osteoblasts and the prevention of osteoblast apoptosis. However, treatment with dexamethasone is thought to destabilize and inhibit nuclear translocation of ß-catenin, decreasing the survival of osteoblasts. By using precursor mouse osteoblast MC3T3 cells, we will analyze antisense morpholino oligonucleotide targeted to Col11a1 as a potential treatment to reverse or block the detrimental effects of dexamethasone on the wnt signaling pathway. MC3T3 cells will be exposed to different treatments in vitro, then aspects of the cell cycle will be analyzed by markers of apoptosis, specific signaling pathways, and cell proliferation rates. While the data obtained in this experiment is relevant to human cell functioning, future research with human cells will strengthen this line of investigation further and establish greater relevance to human health.
Halla, Fabio; Jennings, Emmie; Oxford, Julia; Tuft, Stephanie; and Fujimoto, Akina, "Cell Model System for Glucocorticoid-Induced Osteoporosis" (2020). 2020 Undergraduate Research Showcase. 74.