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LncRNA RMRP Contributes to the Development and Progression of Spinal Cord Injury by Regulating miR-766-5p/FAM83A Axis
Molecular Neurobiology ( IF 5.1 ) Pub Date : 2022-07-28 , DOI: 10.1007/s12035-022-02968-3
Hongxiang Hong 1 , Guanhua Xu 1 , JiaJia Chen 1 , Jinlong Zhang 1 , Chu Chen 1 , Chunshuai Wu 1 , Jiawei Jiang 1 , Zhiming Cui 1
Affiliation  

Spinal cord injury (SCI) is known as a central nervous system disorder. Previous studies suggested that long-non-coding RNA RMRP (LncRNA RMRP) was abnormally expressed in SCI, but the potential underlying mechanism remains to be further explored. To explore the regulatory roles of LncRNA RMRP/miR-766-5p/FAM83A axis in SCI. Spinal T9 hemisection was performed on healthy adult male Sprague Dawley (SD) rats to establish the SCI rat models. The expressions of LncRNA RMRP in spinal cord of rats in different groups were examined by RT-qPCR. Moreover, AGE1.HN and PC12 cells were treated with hypoxic condition, and expression of LncRNA RMRP was examined by RT-qPCR methods. Furthermore, hypoxic PC12 cells were transfected with LncRNA RMRP OE, and the cell viability, proliferation, and apoptosis were examined. Next, the direct targeting relationship between LncRNA RMRP and miR-766-5p, as well as miR-766-5p and FAM83A, was confirmed by dual-luciferase reporter and RNA pull-down assays. Finally, the effects of LncRNA RMRP/miR-766-5p/FAM83A axis on cell viability, proliferation, and apoptosis were examined. LncRNA RMRP was downregulated in SCI rats and over-expression of LncRNA RMRP alleviated the SCI condition. LncRNA RMRP over-expression increased the viability and proliferation, and inhibited the apoptosis of hypoxic PC12 cells in vitro. miR-766-5p was confirmed as a target of LncRNA RMRP, and FAM83A was confirmed as a target of miR-766-5p. LncRNA RMRP could regulate the proliferation and apoptosis of hypoxic PC12 cells via regulating miR-766-5p/FAM83A axis in vitro. LncRNA RMRP may contribute to the pathogenesis of SCI via regulating miR-766-5p/FAM83A axis.



中文翻译:

LncRNA RMRP 通过调节 miR-766-5p/FAM83A 轴促进脊髓损伤的发生和进展

脊髓损伤 (SCI) 被称为中枢神经系统疾病。先前的研究表明,长链非编码RNA RMRP(LncRNA RMRP)在SCI中异常表达,但潜在的潜在机制仍有待进一步探索。探讨LncRNA RMRP/miR-766-5p/FAM83A轴在SCI中的调控作用。对健康成年雄性 Sprague Dawley (SD) 大鼠进行脊髓 T9 半切,以建立 SCI 大鼠模型。RT-qPCR检测不同组大鼠脊髓中LncRNA RMRP的表达。此外,AGE1.HN和PC12细胞在缺氧条件下处理,通过RT-qPCR方法检测LncRNA RMRP的表达。此外,用LncRNA RMRP OE转染缺氧的PC12细胞,检测细胞活力、增殖和凋亡。下一个,LncRNA RMRP 和 miR-766-5p 以及 miR-766-5p 和 FAM83A 之间的直接靶向关系通过双荧光素酶报告基因和 RNA 下拉分析得到证实。最后,检测了 LncRNA RMRP/miR-766-5p/FAM83A 轴对细胞活力、增殖和凋亡的影响。LncRNA RMRP 在 SCI 大鼠中下调,LncRNA RMRP 的过表达缓解了 SCI 状况。LncRNA RMRP过表达增加了体外的活力和增殖,并抑制了缺氧PC12细胞的凋亡。miR-766-5p 被确认为 LncRNA RMRP 的靶标,FAM83A 被确认为 miR-766-5p 的靶标。LncRNA RMRP可通过体外调控miR-766-5p/FAM83A轴调控缺氧PC12细胞的增殖和凋亡。LncRNA RMRP 可能通过调节 miR-766-5p/FAM83A 轴参与 SCI 的发病机制。

更新日期:2022-07-30
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