Researcher(s)
- Dakota Jankovic, Biological Sciences, University of Delaware
Faculty Mentor(s)
- Anja Nohe, Biological Sciences, University of Delaware
Abstract
Osteoporosis (OP) is a bone disease that results from the chronic degradation of trabecular bone tissue due to an imbalance in the bone remodeling system, which skews normal bone homeostasis toward the breakdown and resorption of bone by osteoclasts. These cells, responsible for removing old bone, outpace the activity of osteoblasts in forming new bone, typically causing this shift in osteoclastic versus osteoblastic activity to occur with increased age. As this imbalance progresses, bone mineral density (BMD) and mass decrease, forming larger pores in the trabecular bone, compromising its structural integrity and leading to OP. Bone morphogenetic protein-2 (BMP-2) is an essential growth factor secreted by osteoblasts and their mature forms, known as osteocytes, which induces bone formation. BMP-2 is expressed during early stages of embryonic development and continues to play an important role in bone remodeling throughout an organism’s life. The aim of my summer research project was to determine which signaling pathways were transduced following the stimulation of C2C12 myoblast cells. — a wild-type (WT) group, which is genetically unmodified, and a bone morphogenetic protein receptor type 1a knockout (BMPR1a KO) group, that has the BMPR1a gene knocked out — with two varying concentrations, 40nM and 200nM, of BMP2 for 18 hours. I hypothesized that BMP2 stimulation in cells lacking BMPR1a will only activate non-canonical signaling pathways, as BMPRII cannot form the heterodimeric complex needed for SMAD signaling, without BMPR1a. To determine which signaling cascade was used by the cell, a western blot analysis was performed to determine which signaling molecules were phosphorylated.
- There is data still currently being collected and this abstract will be updated once the results are in, thank you for your patience!