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Positive Feedback Loop LINC00511/miR-150-5p/SP1 Modulates Chondrocyte Apoptosis and Proliferation in Osteoarthritis

机译:阳性反馈环LINC00511 / miR-150-5P / SP1调节软骨细胞凋亡和骨关节炎的增殖

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摘要

Osteoarthritis (OA) acts as the most common type of degenerative joint disease. Long noncoding RNA (lncRNA) has been identified to regulate the apoptosis and proliferation of chondrocyte. However, the deepgoing mechanism involved in the regulation is still unclear. This research aims to investigate the role and molecular mechanism by which lncRNA LINC00511 regulates the OA biology. Functionally, the functional experiments found that LINC00511 expression was upregulated in the IL-1 beta-stimulated chondrocyte (ATDC5). Knockdown of LINC00511 facilitated proliferation, and repressed the apoptosis and extracellular matrix (ECM) synthesis of chondrocyte. Mechanically, LINC00511 functioned as sponge of miR-150-5p and then interacted with the 3 '-UTR of transcription factor (SP1). In turn, transcription factor SP1 bound with the promoter region of LINC00511 and thus upregulated LINC00511 expression. In conclusion, our findings highlight the function and prognostic value of LINC00511/miR-150-5p/SP1 feedback loop in OA and extend the importance of lncRNA epigenetics in OA biology.
机译:骨关节炎(OA)充当最常见的退行性关节疾病。已经鉴定了长的非分量RNA(LNCRNA)以调节软骨细胞的凋亡和增殖。然而,调节中涉及的深度机制仍然不清楚。该研究旨在探讨LNCRNA LINC00511调节OA生物学的作用和分子机制。在功能上,功能实验发现,在IL-1β刺激的软骨细胞(ATDC5)中上调LINC00511表达。 LINC00511的敲低促进增殖,并压制细胞凋亡和细胞外基质(ECM)合成软骨细胞。机械地,LINC00511用作miR-150-5p的海绵,然后用转录因子(SP1)的3'-FUTR相互作用。反过来,转录因子SP1与LINC00511的启动子区结合,因此上调的LINC00511表达。总之,我们的研究结果突出了OA中LINC00511 / MIR-150-5P / SP1反馈环路的功能和预后值,并扩展了LNCRNA表观遗传学在OA生物学中的重要性。

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