Optimizing the Concentration of Peptide CK2.1 for Chondrogenesis in Primary Cells from Patients with Osteoarthritis and Osteoporosis

• Kailey DeGeorge, Biological Sciences, University of Delaware

• Anja Nohe, Biological Sciences, University of Delaware

Osteoarthritis (OA) is a degenerative illness caused by mechanical stress slowly leading to the degradation of cartilage at the joints. Specifically, OA causes the loss of cartilage cells, known as chondrocytes, as well as the breakdown of collagen fibers and the decrease of proteoglycan content. Osteoporosis, another common disease of the musculoskeletal system, is characterized primarily by low bone mass and the subsequently elevated risk of fractures. Currently, there is no known cure for either OA or OP. The growth factor Bone Morphogenetic Protein-2 has been shown to induce the growth and proliferation of chondrocytes and therefore has potential as a therapeutic for OA. However, BMP2 has also been demonstrated to cause harmful side effects, such as chondrocyte hypertrophy. A novel peptide, Casein Kinase 2, has been shown to interact with the Bone Morphogenetic Protein Receptor Type Ia (BMPRIa) in a similar manner to BMP2. The peptide CK2.1 in particular has been shown to induce chondrogenesis. In this experiment, chondrocytes were isolated from the femoral heads of patient samples and stimulated with varying concentrations of CK2.1, then stained with Alcian blue dye. The dye binds to proteoglycans; a darker stain indicates a higher concentration of proteoglycans and therefore a proliferation of chondrocytes. The goal is to determine at what concentration CK2.1 can facilitate cartilage growth most effectively. Cells from three OA and two OP patients were used. Images of the cells were taken and processed using ImageJ. Our results demonstrate that 100 to 250nm is the ideal concentration of CK2.1 for chondrocyte proliferation in OA. The effect of CK2.1 on the OP chondrocytes were found to be inconclusive. Our findings demonstrate that CK2.1 is a potential therapeutic for OA, while more research must be done to investigate the effect of CK2.1 on OP chondrocytes.