Knockdown of circ-PRKCH alleviates IL-1β-treated chondrocyte cell phenotypic changes through modulating miR-502-5p/ADAMTS5 axis.

BACKGROUND

Osteoarthritis (OA) is a common joint disease characterized by progressive cartilage degradation. Circular RNAs (circRNAs) are involved in the initiation and development of OA. This study aimed to explore the potential role and mechanism of circRNA protein kinase C eta (circ-PRKCH) in OA.

METHODS

A total of 30 cartilage specimens were collected from OA patients or normal subjects. Human chondrocytes (CHON-001) were stimulated with interleukin-1β (IL-1β) to establish an

RESULTS

Circ-PRKCH and ADAMTS5 expression levels were up-regulated, while miR-502-5p expression was down-regulated in OA cartilage tissues and IL-1β-treated chondrocytes. Depletion of circ-PRKCH relieved IL-1β-treated chondrocyte cell phenotypic changes by promoting cell proliferation and migration, as well as inhibiting apoptosis and inflammatory response. Mechanically, circ-PRKCH acted as a sponge for miR-502-5p to regulate ADAMTS5 expression, thereby contributing to IL-1β-treated chondrocyte cell phenotypic changes. Moreover, exosomes derived from IL-1β-treated chondrocytes could transfer circ-PRKCH across cells.

CONCLUSION

Circ-PRKCH contributed to IL-1β-treated cell phenotypic changes in chondrocytes