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Expression of miR-204 in patients with osteoarthritis and its damage to chondrocytes

OBJECTIVE: To explore the expression of miR-204 in patients with Osteoarthritis (OA) and its effect on chondrocytes. METHODS: Cartilage tissues of patients with OA, and normal cartilage tissues of patients receiving emergent traumatic amputation were collected. Polymerase chain reaction (PCR) was us...

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Detalles Bibliográficos
Autores principales: Liu, Xiaodong, Gao, Feng, Wang, Weikang, Yan, Jinglong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: International Society of Musculoskeletal and Neuronal Interactions 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7288379/
https://www.ncbi.nlm.nih.gov/pubmed/32481242
Descripción
Sumario:OBJECTIVE: To explore the expression of miR-204 in patients with Osteoarthritis (OA) and its effect on chondrocytes. METHODS: Cartilage tissues of patients with OA, and normal cartilage tissues of patients receiving emergent traumatic amputation were collected. Polymerase chain reaction (PCR) was used to quantify the expressions of miRNAs. Chondrocytes of patients with OA were isolated, cultured, and transfected with miR-204 mimics or miR-204 inhibitor, and cell models of over-expression and knockdown of miR-204 were constructed. MTT assay, clone formation test, trypan blue staining, and TdT-mediated dUTP Nick-End Labeling (TUNEL) staining were used to detect the effect of overexpression or knockdown of miR-204 on viability, proliferation, survival rate and apoptosis of chondrocytes. RESULTS: miR-204 expression increased significantly in cartilage tissue of patients with OA. Results of MTT assay, clone formation test, and trypan blue staining showed that the over-expression of miR-204 inhibited the viability, proliferation, and survival rate, as well as promoted the apoptosis of chondrocytes. Whereas the knockdown of miR-204 improved the viability, proliferation, and survival rate of chondrocytes. CONCLUSION: The expression of miR-204 increased significantly in patients with OA and played a damaging role in chondrocytes. The knockdown of miR-204 may provide new approaches for clinical treatment of OA.