Hsa_circ_0032131 knockdown inhibits osteoarthritis progression via the miR-502-5p/PRDX3 axis

Abstract

Osteoarthritis (OA) is a chronic disease characterized by progressive loss of cartilage and failure of the diarthrodial joint. Circular RNAs (circRNAs) are known to participate in the pathogenesis of multiple diseases, including OA. We investigated the functions of hsa_circ_0032131, a circRNA upregulated in OA, using CHON-001 cells and an <i>in vivo</i> OA rat model. CHON-001 cells were treated with interleukin (IL)-1β to mimic OA <i>in vitro.</i> IL-1β-induced inhibition of CHON-001 growth was reversed by silencing hsa_circ_0032131. In addition, hsa_circ_0032131 knockdown reversed IL-1β-induced activation of Trx1, Cyclin D and PRDX3, whereas overexpression of <i>PRDX3</i>, a direct target of miR-502-5p, reversed this effect. Hsa_circ_0032131 served as a competing endogenous RNA for miR-502-5p. Moreover, knockdown of hsa_circ_0032131 attenuated OA symptoms <i>in vivo</i> by inactivating the STAT3 signaling pathway. Thus, silencing of hsa_circ_0032131 inhibited the progression of OA by inactivating the miR-502-5p/PRDX3/Trx1/STAT3 axis, which highlights its potential as a therapeutic target for OA.