Background

Osteoarthritis (OA) is a degenerative joint disease involving the cartilage and many of its surrounding tissues (Martel-Pelletier et al., 2016). Patients with OA experience pain, joint stiffness in the early stage, and even suffering disability in the later stage (Abramoff & Caldera, 2020). At present, the therapeutic strategy of OA is limited, mainly including pain reduction and anti-inflammation, which fail to prevent and delay the progress of OA (Bijlsma, Berenbaum, & Lafeber, 2011). And surgical treatment brings a lot of burden to patients, especially the elderly (Litwic, Edwards, Dennison, & Cooper, 2013). Thus, its urgent to develop new strategies for the treatment of OA.

Osteoarthritis of the knee (left) and the hip (right), via Wikimedia Commons

Osteoglycin (OGN) is a proteoglycan released from bone and muscle which is involved in extracellular matrix metabolism (Tanaka et al., 2012). Recent studies have found that the expression of OGN is significantly reduced in the articular cartilage of patients with OA (Balakrishnan et al., 2014). As the only cell type in the articular cartilage, chondrocytes can express and secrete large amounts of extracellular matrix including collagen and polysaccharide, which play an important role in the maintenance of cartilage homeostasis (Carballo, Nakagawa, Sekiya, & Rodeo, 2017). However, the regulatory role of OGN in chondrocytes remains unclear.

Design

Since the expression of OGN is significantly reduced in the articular cartilage of patients with OA, we first investigated the effect of IL-1β on the expression of OGN in chondrocytes. We next used genetic engineering techniques to construct OGN overexpressed and silencing plasmids and determined the effect of OGN expression change on the matrix metabolism of chondrocytes. Based on the results of the above experiments, we evaluated the possibility of OGN as a therapeutic target for OA treatment.

References

Abramoff, B., & Caldera, F. E. (2020). Osteoarthritis: Pathology, Diagnosis, and Treatment Options. Med Clin North Am, 104(2), 293-311. doi:10.1016/j.mcna.2019.10.007

Balakrishnan, L., Nirujogi, R. S., Ahmad, S., Bhattacharjee, M., Manda, S. S., Renuse, S., . . . Pandey, A. (2014). Proteomic analysis of human osteoarthritis synovial fluid. Clin Proteomics, 11(1), 6. doi:10.1186/1559-0275-11-6

Bijlsma, J. W., Berenbaum, F., & Lafeber, F. P. (2011). Osteoarthritis: an update with relevance for clinical practice. Lancet, 377(9783), 2115-2126. doi:10.1016/S0140-6736(11)60243-2

Carballo, C. B., Nakagawa, Y., Sekiya, I., & Rodeo, S. A. (2017). Basic Science of Articular Cartilage. Clin Sports Med, 36(3), 413-425. doi:10.1016/j.csm.2017.02.001

Litwic, A., Edwards, M. H., Dennison, E. M., & Cooper, C. (2013). Epidemiology and burden of osteoarthritis. Br Med Bull, 105, 185-199. doi:10.1093/bmb/lds038

Martel-Pelletier, J., Barr, A. J., Cicuttini, F. M., Conaghan, P. G., Cooper, C., Goldring, M. B., . . . Pelletier, J. P. (2016). Osteoarthritis. Nat Rev Dis Primers, 2, 16072. doi:10.1038/nrdp.2016.72

Tanaka, K., Matsumoto, E., Higashimaki, Y., Katagiri, T., Sugimoto, T., Seino, S., & Kaji, H. (2012). Role of osteoglycin in the linkage between muscle and bone. J Biol Chem, 287(15), 11616-11628. doi:10.1074/jbc.M111.292193