Induction of CEMIP in Chondrocytes by Inflammatory Cytokines: Underlying Mechanisms and Potential Involvement in Osteoarthritis

• Published in: International journal of molecular sciences Vol. 21; no. 9; p. 3140
• Main Authors: Ohtsuki, Takashi, Hatipoglu, Omer F, Asano, Keiichi, Inagaki, Junko, Nishida, Keiichiro, Hirohata, Satoshi
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 29.04.2020; MDPI
• Subjects: Arthritis; Biomarkers; Biomedical materials; Cartilage; Cartilage diseases; Cell adhesion & migration; cell migration-inducing hyaluronidase 1 (CEMIP); chondrocyte; Chondrocytes; Chondrocytes - metabolism; Cytokines; Cytokines - metabolism; Depolymerization; Disease Susceptibility; Extracellular matrix; Fibroblasts; Fluorescent Antibody Technique; Gene Expression; Growth factors; Humans; hyaluronan; Hyaluronic acid; Hyaluronoglucosaminidase - genetics; Hyaluronoglucosaminidase - metabolism; IL-1β; Immunohistochemistry; Inflammation; Inflammation Mediators - metabolism; Mechanical stimuli; mechanical strain; Metabolism; Molecular weight; NF-κB protein; nuclear factor kappa B (NF-κB); Nuclear transport; Osteoarthritis; Osteoarthritis - etiology; Osteoarthritis - metabolism; Osteoarthritis - pathology; Phosphorylation; Protein expression; Proteins; Signal transduction; Stress, Mechanical; Synovial fluid; Tumor necrosis factor-TNF; mechanical strain; chondrocyte; nuclear factor kappa B (NF-κB); hyaluronan; osteoarthritis; cell migration-inducing hyaluronidase 1 (CEMIP)
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms21093140

In patients with osteoarthritis (OA), there is a decrease in both the concentration and molecular size of hyaluronan (HA) in the synovial fluid and cartilage. Cell migration-inducing hyaluronidase 1 (CEMIP), also known as hyaluronan (HA)-binding protein involved in HA depolymerization (HYBID), was recently reported as an HA depolymerization-related molecule expressed in the cartilage of patients with OA. However, the underlying mechanism of CEMIP regulation is not well understood. We found that CEMIP expression was transiently increased by interleukine-1β (IL-1β) stimulation in chondrocytic cells. We also observed that ERK activation and NF-κB nuclear translocation were involved in the induction of CEMIP by IL-1β. In addition, both administration of HA and mechanical strain attenuated the CEMIP induction in IL-1β-stimulated chondrocytes. In conclusion, we clarified the regulatory mechanism of CEMIP in chondrocytes by inflammatory cytokines and suggested the potential involvement in osteoarthritis development.