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Targeted overexpression of the long noncoding RNA ODSM can regulate osteoblast function in vitro and in vivo

机译:长度非划分RNA ODSM的靶向过度表达可以在体外和体内调节成骨细胞功能

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Ameliorating bone loss caused by mechanical unloading is a substantial clinical challenge, and the role of noncoding RNAs in this process has attracted increasing attention. In this study, we found that the long noncoding RNA osteoblast differentiation-related lncRNA under simulated microgravity (lncRNA ODSM) could inhibit osteoblast apoptosis and promote osteoblast mineralization in vitro. The increased expression level of the lncRNA ODSM partially reduced apoptosis and promoted differentiation in MC3T3-E1 cells under microgravity unloading conditions, and the effect was partially dependent on miR-139-3p. LncRNA ODSM supplementation in hindlimb-unloaded mice caused a decrease in the number of apoptotic cells in bone tissue and an increase in osteoblast activity. Furthermore, targeted overexpression of the lncRNA ODSM in osteoblasts partially reversed bone loss induced by mechanical unloading at the microstructural and biomechanical levels. These findings are the first to suggest the potential value of the lncRNA ODSM in osteoporosis therapy and the treatment of pathological osteopenia.
机译:由机械卸载引起的改善骨质损失是一个大量的临床挑战,并且非编码RNA在该过程中的作用引起了越来越关注。在该研究中,我们发现,在模拟微匍匐(LNCRNA ODSM)下的长度非编码RNA成骨细胞分化相关的LNCRNA可以抑制成骨细胞凋亡并在体外促进成骨细胞矿化。 LNCRNA ODSM的表达水平的增加部分降低了微生物卸载条件下MC3T3-E1细胞中的细胞凋亡和促进分化,并且效果部分依赖于miR-139-3p。 LNCRNA ODSM补充在后肢 - 卸载的小鼠中导致骨组织中凋亡细胞数量的减少和成骨细胞活性的增加。此外,在成骨细胞中的LNCRNA ODSM的靶向过度表达部分地反转通过机械卸载在微观结构和生物力学水平上诱导的骨质损失。这些发现是第一个提出骨质疏松症治疗中LNCRNA ODSM的潜在价值和病理骨质脑病的治疗。

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