Knockdown of circSOD2 ameliorates osteoarthritis progression via the miR-224-5p/PRDX3 axis.
J Orthop Surg Res
; 18(1): 432, 2023 Jun 13.
Article
en En
| MEDLINE
| ID: mdl-37312219
BACKGROUND: Although the implications of circular RNAs (circRNAs) with the progression of diverse pathological conditions have been reported, the circRNA players in osteoarthritis (OA) are barely studied. METHODS: In this study, twenty-five OA patients who received arthroplasty were recruited for cartilage tissue collection. Public circRNA microarray data from Gene Expression Omnibus was retrieved for circRNA identification. An in vitro cell model of OA-related damages was constructed by treating human chondrocytes (CHON-001 cell line) with IL-1ß, and circSOD2 siRNA was used to silence circSOD2 expression to study its functional role in apoptosis, inflammatory responses, and extracellular matrix (ECM) degradation. Besides, we investigated the functional interactions among circSOD2, miR-224-5p, and peroxiredoxin 3 (PRDX3) by luciferase reporter assay, RNA-immunoprecipitation assay, and quantitative reverse transcription polymerase chain reaction. RESULTS: Our findings revealed the overexpression of circSOD2 in the OA cartilage and cell samples, and circSOD2 knockdown alleviated ECM degradation, inflammation, and apoptosis in CHON-001 cell model. In addition, our findings suggested the regulatory function of circSOD2 knockdown on miR-224-5p expression, while miR-224-5p was capable of downregulating PRDX3 expression. The co-transfection of miR-224-5p inhibitor or pcDNA-PRDX3 could prevent the effect of circSOD2 knockdown. CONCLUSION: Hence, our results demonstrated that knockdown of circSOD2 may serve as an intervention strategy to alleviate OA progression through modulating miR-224-5p/PRDX3 signaling axis.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Osteoartritis
/
MicroARNs
Tipo de estudio:
Prognostic_studies
Límite:
Humans
Idioma:
En
Revista:
J Orthop Surg Res
Año:
2023
Tipo del documento:
Article
País de afiliación:
China
Pais de publicación:
Reino Unido