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• W2770426276 abstract "To investigate whether microRNA-24 (miR-24) targeting C-myc affects chondrocytes of rats with osteoarthritis (OA) via the MAPK signaling pathway. Thirty rats were assigned as a sham group and an OA group (established as OA rat models by cutting the anterior cruciate ligaments and removing 1/3 medial meniscus). TUNEL staining and immunohistochemistry were conducted for cell apoptosis index (AI) and positive expression rate of C-myc protein. Enzyme-linked immuno sorbent assay (ELISA) was carried out for serum level of IL-1β and TNF-α. Primary chondrocytes were assigned into the blank, negative control (NC), miR-24 mimics, miR-24 inhibitors, siRNA-C-myc, and miR-24 inhibitors+siRNA-C-myc groups. The expressions of miR-24, C-myc, p38, ERK, JNK, IL-1β, and TNF-α in tissues and cells were detected using reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR) and Western blotting. CCK8 assay and flow cytometry were performed for cell proliferation and apoptosis. The OA group showed higher IL-1β, TNF-α, AI, and C-myc than the sham group. C-myc is a target gene of miR-24. Compared with the blank group, the miR-24 mimics and siRNA-C-myc groups showed reduced expression of C-myc, IL-1β, TNF-α, p38, p-p38, ERK, p-ERK, JNK, and p-JNK, apoptosis rate yet increased cell proliferation; however, the miR-24 inhibitors group exhibited an opposite trend. The miR-24 inhibitors+siRNA-C-myc group presented a same tendency compared to the siRNA-C-myc group. Upregulated miR-24 downregulates C-myc could suppress apoptosis and promote proliferation of chondrocytes to prevent the occurrence and subsequent progression of OA via inactivating the MAPK signaling pathway." @default.
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• W2770426276 date "2017-09-11" @default.
• W2770426276 modified "2023-10-15" @default.
• W2770426276 title "<i>Retracted</i>: Effects of microRNA‐24 targeting <i>C‐myc</i> on apoptosis, proliferation, and cytokine expressions in chondrocytes of rats with osteoarthritis via MAPK signaling pathway" @default.
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• W2770426276 doi "https://doi.org/10.1002/jcb.26514" @default.
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