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


  • Kailey DeGeorge, Biological Sciences, University of Delaware

Faculty Mentor(s)

  • 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. However, it has also been demonstrated to cause harmful side effects. The novel peptide CK2.1 has been shown to release casein kinase II (CK2) from sites at the Bone Morphogenetic Protein Receptor Type Ia (BMPRIa) and thereby activate BMP signaling in a similar manner to BMP2. The peptide CK2.1 has previously been shown to induce chondrogenesis and cartilage activity in this manner in mouse models. The objective of this experiment is to stimulate primary chondrocytes from patients diagnosed with OA to determine which concentrations, if any, induce chondrogenesis and chondrocyte activity in human primary cells. Cells from patients diagnosed with OP were also stimulated with CK2.1 and served as the control, as OP affects bone but cartilage remains healthy.