Liu Sen, Cui Bei, Dai Zhen-xia, Shi Peng-ke, Wang Zhao-hui, Guo Yuan-yuan
Institute: Department of Neurology, Huaihe Hospital of Henan University, Kaifeng, Henan 475000, P. R. China.
Curr Neurovasc Res. 2016;13(2):115-20. doi: 10.2174/1567202613666160316155228.
Homeobox (HOX) transcript antisense RNA (HOTAIR), as a long intergenic noncoding RNA (lincRNA), is known to be overexpressed in several cancers. However, the role of HOTAIR in Parkinson's disease (PD) remains unclear. A mouse model of PD was developed by intraperitoneal injection of MPTP (N-methyl-4-phenyl-1,2,3,6- tetrahydropyridine). The expression of HOTAIR and LRRK2 (leucine-rich repeat kinase 2) were detected in the PD mice and in Human neuroblastoma cell lines SH-SY5Y pretreated with MPP+ (N-methyl-4-phenylpyridinium). The effect of HOTAIR on the expression of LRRK2 was examined in SH-SY5Y cells through overexpressing HOTAIR. A MTT (3- (4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide) assay was performed to measure the cell viability of SH-SY5Y cells. si-HOTAIR (siRNA-HOTAIR) was utilized to investigate the effect of HOTAIR on the expression of LRRK2 in vivo. In this study, upregulation of HOTAIR and LRRK2 were found in the midbrain of PD mice induced by MPTP and in SH-SY5Y cells pretreated with MPP+. With the presence of HOTAIR overexpression in SH-SY5Y cells, the expression of LRRK2 was increased compared with that in the control. HOTAIR knockdown showed a protective effect on the cell viability of SH-SY5Y cells pretreated with MPP+, which was abrogated by overexpression of LRRK2. In mouse model of PD treated with si-HOTAIR, the expression of LRRK2 was decreased. In conclusion, high expression of HOTAIR promoted the onset of PD induced by MPTP. Moreover, the finding that HOTAIR promoted PD induced by MPTP through regulating LRRK2 expression could add our understanding of the molecular mechanisms in PD.
同源框(HOX)转录反义RNA(HOTAIR)作为一种长链基因间非编码RNA(lincRNA),在多种癌症中均有过表达。然而,HOTAIR在帕金森病(PD)中的作用仍不清楚。通过腹腔注射MPTP(N-甲基-4-苯基-1,2,3,6-四氢吡啶)建立了PD小鼠模型。检测了PD小鼠以及用MPP +(N-甲基-4-苯基吡啶鎓)预处理的人神经母细胞瘤细胞系SH-SY5Y中HOTAIR和富含亮氨酸重复激酶2(LRRK2)的表达。通过过表达HOTAIR在SH-SY5Y细胞中检测HOTAIR对LRRK2表达的影响。进行MTT(3-(4,5-二甲基-2-噻唑基)-2,5-二苯基-2-H-四唑溴盐)试验以测量SH-SY5Y细胞的活力。利用si-HOTAIR(siRNA-HOTAIR)研究HOTAIR在体内对LRRK2表达的影响。在本研究中,发现MPTP诱导的PD小鼠中脑以及用MPP +预处理的SH-SY5Y细胞中HOTAIR和LRRK2上调。在SH-SY5Y细胞中过表达HOTAIR时,与对照相比,LRRK2的表达增加。HOTAIR敲低对用MPP +预处理的SH-SY5Y细胞的活力具有保护作用,而LRRK2的过表达可消除这种保护作用。在用si-HOTAIR处理的PD小鼠模型中,LRRK2的表达降低。总之,HOTAIR的高表达促进了MPTP诱导的PD的发生。此外,HOTAIR通过调节LRRK2表达促进MPTP诱导的PD这一发现,有助于我们对PD分子机制的理解。