Osteoarthritis (OA) is characterized by degradation of chondrocyte extracellular matrix (ECM). Accumulating evidence suggests that microRNAs (miRNAs) are associated with OA, but little is known of their function in chondrocyte ECM degradation. The objective of this study was to investigate the expression and function of miRNAs in OA. miRNA expression profile was determined in OA cartilage tissues and controls, employing Solexa sequencing and reverse transcription quantitative PCR (RT-qPCR). According to a modified Mankin scale, cartilage degradation was evaluated. Functional analysis of the miRNAs on chondrocyte ECM degradation was performed after miRNA transfection and IL-1β treatment. Luciferase reporter assays and western blotting were employed to determine miRNA targets. Expression of miR-221-3p was downregulated in OA cartilage tissues, which was significantly correlated with a modified Mankin scale. Through gain-of-function and loss-of-function studies, miR-221-3p was shown to significantly affect matrix synthesis gene expression and chondrocyte proliferation and apoptosis. Using SW1353 and C28I2 cells, SDF1 was identified as a target of miR-221-3p. SDF1 overexpression resulted in increased expression of catabolic genes such as MMP-13 and ADAMTS-5 in response to IL-1β, but these effects were moderated by miR-221-3p. SDF1 treatment antagonized this effect, while knockdown of SDF1 by shSDF1 induced inhibitory effects on the expression of CXCR4 and its main target genes, similar to miR-221-3p. The results indicate that upregulation of miR-221-3p could prevent IL-1β-induced ECM degradation in chondrocytes. Targeting the SDF1/CXCR4 signaling pathway may be used as a therapeutic approach for OA. miR-221-3p is downregulated in human cartilage tissues. miR-221-3p levels are associated with cartilage degeneration grade. miR-221-3p upregulation prevents IL-1β-induced ECM degradation in chondrocytes. Protection of ECM degradation by miR-223-3p occurs via SDF1/CXCR4 signaling. miR-221-3p is identified as a novel potential therapeutic target for osteoarthritis. KEY MESSAGES: miR-221-3p is downregulated in human cartilage tissues. miR-221-3p levels are associated with cartilage degeneration grade. miR-221-3p upregulation prevents IL-1β-induced ECM degradation in chondrocytes. Protection of ECM degradation by miR-223-3p occurs via SDF1/CXCR4 signaling. miR-221-3p is identified as a novel potential therapeutic target for osteoarthritis.

Closure with running subcuticular suture is cheaper and appears to have a clinical advantage when compared with metallic staples skin closure in primary THA surgery. However, additional operating time may be incurred.

Background Long non-coding RNA (LncRNA) TUG1 plays critical roles in the development of human cancers. Its inhibition has been proved to participate in ankylosing spondylitis, which is an inverse pathological procedure of osteoporosis. In the present study, we aim to investigate the role of lncRNA TUG1 in ankylosing spondylitis. Materials and methods Expressions of lncRNA TUG1 in plasma of 98 patients with osteoporosis and 60 healthy participants were detected by real-time quantitative PCR (RT-qPCR). Diagnostic values of lncRNA CASC11 for osteoclasts were performed by the ROC curve with osteoporosis patients as positive and healthy participants as negative. All experiments were repeated 3 times. Mean ± standard deviation was calculated. Results We found that plasma lncRNA TUG1 was upregulated in osteoporosis patients than in healthy participants. Upregulation of plasma lncRNA TUG1 distinguished osteoporosis patients from healthy participants. LncRNA TUG1 level increased with the advances of clinical stages. Over-expression of lncRNA TUG1 promoted the proliferation and inhibited the apoptosis of mice osteoclasts, while lncRNA TUG1 siRNA silencing played an opposite role. In addition, lncRNA TUG1 over-expression led to downregulated PTEN, while lncRNA TUG1 siRNA silencing played an opposite role. Conclusion Therefore, lncRNA TUG1 is upregulated in osteoporosis and regulates the proliferation and apoptosis of osteoclasts. lncRNA TUG1 knockdown may serve as a promising therapeutic target for osteoporosis by inhibiting the proliferation and promoting the apoptosis of osteoclasts through PTEN.

Objectives We investigated the role of long non-coding (lnc) RNA-NEF (neighboring enhancer of FoxA2), a characterized oncogene in cancer biology, in postmenopausal osteoporosis and its diagnostic and prognostic value in this disease. Methods Expression of lncRNA-NEF in plasma was detected by RNA extraction and real-time quantitative PCR. The diagnostic value of lncRNA-NEF and interleukin (IL)-6 for postmenopausal osteoporosis was evaluated by receiver operating characteristic curve analysis, with postmenopausal osteoporosis patients as true positive cases and healthy volunteers as true negative cases. Results We showed that plasma lncRNA-NEF was downregulated and plasma IL-6 was upregulated in postmenopausal osteoporosis patients compared with healthy controls. Altered plasma levels of lncRNA-NEF and IL-6 separated postmenopausal osteoporosis patients from healthy controls, and lncRNA-NEF and IL-6 were inversely and significantly correlated in osteoporosis patients. Patients were divided into high (n = 68) and low lncRNA-NEF (n = 73) groups according to Youden’s index. Patients with high lncRNA-NEF levels required a significantly shorter treatment course and had a lower post-treatment recurrence rate. Conclusion We showed that lncRNA-NEF is downregulated in postmenopausal osteoporosis and is related to course of treatment and recurrence. The involvement of lncRNA-NEF in postmenopausal osteoporosis is likely related to IL-6.

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