Decreased expression of miR-9 due to E50K OPTN mutation causes disruption of the expression of BDNF leading to RGC-5 cell apoptosis

Decreased expression of miR-9 due to E50K OPTN mutation causes disruption of the expression of BDNF leading to RGC-5 cell apoptosis
复制标题

DOI:
10.3892/mmr.2016.5810
复制
发表时间:
2016-11-01
影响因子:
3.4
通讯作者:
Yuan, Huiping
Yuan, Huiping
中科院分区:
医学4区
文献类型:
--
作者:
Jiang, Bo;Gao, Lin;Yuan, Huiping

文献摘要

被引文献

相似文献

本研究的目的是研究E50 K视神经磷酸酶(OPTN)突变对RGC-5细胞的影响,并确定microRNA-9(miR-9)在该系统中的作用。使用转染的RGC-5细胞来评估E50 K OPTN对miR-9表达的影响,并使用蛋白质印迹分析随后对RGC-5细胞凋亡的破坏。结果显示,E50 K OPTN的表达与E50 K OPTN转染的RGC-5细胞中miR-9水平的显著降低相关。miR-9的E50 K OPTN依赖性减少导致转录抑制因子RE 1沉默转录因子的表达增加,并降低脑源性神经营养因子的表达。因此,E50 K OPTN可能会破坏miR-9的表达,提示E50 K OPTN突变可能导致RGC-5细胞凋亡的潜在机制。
The aims of the present study were to investigate the effect of E50K optineurin (OPTN) mutation on RGC-5 cells and to define the role of microRNA-9 (miR-9) in this system. Transfected RGC-5 cells were used to evaluate the effects of E50K OPTN on the expression of miR-9 and subsequent disruption of RGC-5 cell apoptosis was analyzed using western blotting. The results showed that the expression of E50K OPTN was associated with a marked reduction in the levels of miR-9 in the E50K OPTN-transfected RGC-5 cells. The E50K OPTN-dependent reductions in miR-9 led to increased expression of the transcriptional repressor, RE1-silencing transcription factor and decreased the expression of brain-derived neurotrophic factor. Thus, E50K OPTN may disrupt the expression of miR-9, suggesting a potential mechanism by which E50K OPTN mutation may lead to RGC-5 cell apoptosis.