Expressions of miRNAs related to accelerating senescence in serum of patients with amnestic mild cognitive impairment and analysis on their biological information
10.13481/j.1671-587x.20170221
- VernacularTitle:快速老化相关miRNAs在遗忘型轻度认知功能障碍患者血清中的表达及其生物信息学分析
- Author:
Yanwei HUO
;
Bing XIE
;
Lei JIANG
;
Rui ZHANG
;
Mei SONG
;
Lan WANG
;
Xueyi WANG
;
Shunjiang XU
- Keywords:
amnestic mild cognitive impairment;
brain derived neurotrophic factors;
silent information regulator 1;
bioinformatics
- From:
Journal of Jilin University(Medicine Edition)
2017;43(2):322-327
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To explore the expressions of miRNAs related to accelerating senescence in serum of the patients with amnestic mild cognitive impairment (aMCI), and to clarify their effects in the pathogenesis of aMIC.Methods:The levels of miRNAs related to accelerating senescence (miR-132, miR-193b, miR-130b, miR-20a, miR-296, miR-329 and miR-206) were measured in the serum of the patients with aMCI (aMCI group,n=66) and healthy controls(control group,n=76) using quantitative real-time PCR(qRT-PCR).The genes targeted by the altered miRNAs were predicted by TargetScan 6.0.DAVID was used to analyze the function of miRNA target genes.The serum levels of brain derived neurotrophic factor (BDNF) and silent in formation regulator 1(SIRT1) were measured by enzyme-linked immunosorbent assay (ELISA) method.Results:The expression levels of miR-206 and miR-132 in serum of the patients in aMCI group were significantly higher than those in control group (P<0.05).BDNF and SIRT1 were both target genes of miR-206 and miR-132.The levels of BDNF (29.50 μg·L-1± 3.13 μg·L-1) and SIRT1 (1.86 μg·L-1± 0.25 μg·L-1) in serum of the patients in aMCI group were both obviously lower than those in control group (BDNF: 32.29 μg·L-1±3.66 μg·L-1;SIRT1: 2.10 μg·L-1± 0.29 μg·L-1, P<0.05).Conclusion:The expression levels of miR-206 and miR-132 in serum of the aMCI patients are significantly up-regulated.Both of them might be involved in the pathogenesis of aMCI through inhibiting the BDNF and SIRT1 expressions.
