CD24 enrichment protects while its loss increases susceptibility of juvenile chondrocytes towards inflammation ARTHRITIS RESEARCH & THERAPY Lee, J., Smeriglio, P., Dragoo, J., Maloney, W. J., Bhutani, N. 2016; 18


Diseases associated with human cartilage, including rheumatoid arthritis (RA) and osteoarthritis (OA) have manifested age, mechanical stresses and inflammation as the leading risk factors. Although inflammatory processes are known to be upregulated upon aging, we sought to gain a molecular understanding of how aging affects the tissue-specific response to inflammation. In this report, we explored the role of cluster of differentiation 24 (CD24) in regulating differential inflammatory responses in juvenile and adult human chondrocytes.Differential cell-surface CD24 expression was assessed in juvenile and adult chondrocytes along with human induced pluripotent stem cell (hiPSC)-derived neonatal chondrocytes through gene expression and fluorescence-activated cell sorting (FACS) analyses. Loss of function of CD24 was achieved through silencing in chondrocytes and the effects on the response to inflammatory cues were assessed through gene expression and NF?B activity.CD24 expression in chondrocytes caused a differential response to cytokine-induced inflammation, with the CD24(high) juvenile chondrocytes being resistant to IL-1ß treatment as compared to CD24(low) adult chondrocytes. CD24 protects from inflammatory response by reducing NF?B activation, as an acute loss of CD24 via silencing led to an increase in NF?B activation. Moreover, the loss of CD24 in chondrocytes subsequently increased inflammatory and catabolic gene expression both in the absence and presence of IL-1ß.We have identified CD24 as a novel regulator of inflammatory response in cartilage that is altered during development and aging and could potentially be therapeutic in RA and OA.

View details for DOI 10.1186/s13075-016-1183-y

View details for Web of Science ID 000390276900003

View details for PubMedID 27955675

View details for PubMedCentralID PMC5153697