Analysis of serum microRNA expression in male workers with occupational noise-induced hearing loss.
Analysis of serum microRNA expression in male workers with occupational noise-induced hearing loss.
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职业性噪声性听力损失男性工人血清microRNA表达分析
DOI：
10.1590/1414-431x20176426
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发表时间：
2018-01-11
期刊：
影响因子：
--
通讯作者：
Yang L
中科院分区：
文献类型：
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作者：
Li YH;Yang Y;Yan YT;Xu LW;Ma HY;Shao YX;Cao CJ;Wu X;Qi MJ;Wu YY;Chen R;Hong Y;Tan XH;Yang L
职业性噪声性听力损失（ONIHL）是一种常见的职业性疾病，长期暴露于噪声中的工人的听觉功能受损。然而，ONIHL受试者的血清microRNA表达尚未研究。我们旨在比较ONIHL受试者和对照组男性工人的血清microRNA表达谱。microRNA微阵列分析显示，对照组（n=3）和ONIHL受试者（n=3）之间有4种血清microRNA差异表达。在这些microRNA中，ONIHL组中有三种上调（hsa-miR-3162- 5 p、hsa-miR-4484、hsa-miR-1229- 5 p），一种下调（hsa-miR-4652- 3 p）（倍数变化>1.5，Pbon值<0.05）。进行真实的时间定量PCR以验证microRNA表达。与对照组相比，在ONIHL受试者中发现miR-1229- 5 p的血清水平显著增加（每组n=10; P<0.05）。预测共有659个（27.0%）基因为miR-1229- 5 p的靶基因。这些基因参与多种信号通路，如丝裂原活化蛋白激酶（MAPK）信号通路。miR-1229- 5 p过表达显著抑制MAPK 1 3′ UTR片段的荧光素酶活性（P<0.01）。与阴性对照相比，表达miR-1229- 5 p模拟物的HEK 293 T细胞显示MAPK 1的mRNA水平显著下降（P<0.05）。这项初步研究表明，血清miR-1229- 5 p在ONIHL受试者中显著升高。增加的miR-1229- 5 p可能通过抑制MAPK 1信号传导参与ONIHL的发病机制。
Occupational noise-induced hearing loss (ONIHL) is a prevalent occupational disorder that impairs auditory function in workers exposed to prolonged noise. However, serum microRNA expression in ONIHL subjects has not yet been studied. We aimed to compare the serum microRNA expression profiles in male workers of ONIHL subjects and controls. MicroRNA microarray analysis revealed that four serum microRNAs were differentially expressed between controls (n=3) and ONIHL subjects (n=3). Among these microRNAs, three were upregulated (hsa-miR-3162-5p, hsa-miR-4484, hsa-miR-1229-5p) and one was downregulated (hsa-miR-4652-3p) in the ONIHL group (fold change >1.5 and Pbon value <0.05). Real time quantitative PCR was conducted for validation of the microRNA expression. Significantly increased serum levels of miR-1229-5p were found in ONIHL subjects compared to controls (n=10 for each group; P<0.05). A total of 659 (27.0%) genes were predicted as the target genes of miR-1229-5p. These genes were involved in various pathways, such as mitogen-activated protein kinase (MAPK) signaling pathway. Overexpression of miR-1229-5p dramatically inhibited the luciferase activity of 3′ UTR segment of MAPK1 (P<0.01). Compared to the negative control, HEK293T cells expressing miR-1229-5p mimics showed a significant decline in mRNA levels of MAPK1 (P<0.05). This preliminary study indicated that serum miR-1229-5p was significantly elevated in ONIHL subjects. Increased miR-1229-5p may participate in the pathogenesis of ONIHL through repressing MAPK1 signaling.