Differential expression of miR-30a-5p in post stroke depression and bioinformatics analysis of the possible mechanism.
- Author:
Jia HU
1
;
Zhiming ZHOU
1
;
Qian YANG
1
;
Ke YANG
1
Author Information
1. Department of Neurology, Yijishan Hospital Affiliated to Wannan Medical College, Wuhu 241001, China.
- Publication Type:Journal Article
- MeSH:
Brain Ischemia;
Computational Biology;
Depression;
etiology;
genetics;
Gene Expression Regulation, Neoplastic;
Humans;
MicroRNAs;
genetics;
Stroke;
complications
- From:
Journal of Zhejiang University. Medical sciences
2020;40(7):922-929
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the differential expression of miR-30a-5p in patients with poststroke depression and explore the possible mechanism.
METHODS:We obtained the target microRNAs through searching PubMed using the online software VENNY2.1. We collected the baseline demographic, clinical and radiographic data from consecutive patients with first-ever acute ischemic stroke on admission in our department from October, 2018 to March, 2019. From each patient, 5 mL peripheral venous blood was collected upon admission. Hamilton Depression Scale (HAMD-17) was used to evaluate the degree of depression at the end of the 3-month follow-up. The patients with a HAMD-17 score≥7 were diagnosed to have depression according to the diagnostic criteria of the Fourth Edition of the Diagnostic and Statistical Manual of Mental Disorders of the American Psychiatric Association (DSM-IV). The patients were divided into post-stroke depression group (PSD group, =11) and non-post-stroke depression group (non-PSD group, =25), and their plasma levels of miR-30a-5p were detected using qPCR. The STARBASE Database ENCORI miRNA-mRNA module and Comparative Toxicogenomics Database were used to predict and screen the possible target genes related to miR-30a-5p, and the possible mechanism of the target genes was further analyzed through bioinformatics.
RESULTS:miR-30a-5p was identified by cross-screening as the target miRNA associated with stroke and depression and showed obvious differential expression between PSD and non-PSD patients (2.462±0.326 1±0.126, < 0.0001). ROC curve analysis showed that the AUC of miR-30a-5p for predicting PSD was 0.869 (95%: 0.745-0.993, =0.0005) at the cutoff value of 1.597, with a sensitivity and specificity of 0.727 and 0.840, respectively. The target proteins of miR-30a-5p involved a wide range of biological processes, including signal transduction, intercellular communication, regulation of nucleobase, nucleoside, nucleotide and nucleic acid metabolism. KEGG pathway enrichment analysis showed that the target proteins affected mainly the neural nutrient signaling pathway, axon guidance signaling pathway and insulin signaling system. We also identified the top 20 HUB genes that might be associated with post-stroke depression.
CONCLUSIONS:Plasma miR-30a-5p is differentially expressed in PSD and can serve as a new blood marker for diagnosis and also a therapeutic target of PSD.
