Abstract TP276: Identification of Potential Key Genes and Pathways in Ischemic Stroke by Analysis of Human High Throughput Sequencing Data

Abstract

Background and Purpose: Ischemic stroke (IS) is one of the most common causes of human death worldwide, but the molecular mechanisms of IS are still unclear. To explore the key genes and pathways involved in the pathogenic process of IS, we did a bioinformatics analysis of high throughput sequencing data of IS for the first time, which compared the expression profiles of brain tissues in IS patients and health controls. Methods: The dataset SRP040622 analyzed of expression profiling in 13 samples by deep sequencing in the platform of Illumina HiSeq 2000, including seven cortical ischemic stroke tissues and six control cortex tissues. These data from SRP040622 were downloaded from Sequence Read Archive (SRA) by using Prefech. We adopted fastq-dump, Hisat2, samtools, HTseq and DEseq2 to get the quantification of gene expression from raw data. The differentially expressed genes (DEGs) were identified by limma package, and function enrichment analyses were performed in DAVID website. In addition, the protein-protein interaction (PPI) network was constructed by using STRING and Cytoscape. Results: A total 880 DEGs were identified, including 350 up-regulated genes and 530 down-regulated genes. These DEGs enriched in biological processes(BP) mainly associated with signal transduction, multicellular organism development, positive regulation of cell proliferation, protein phosphorylation, cell-cell adhesion and angiogenesis. And KEGG pathway which DEGS were mainly enriched in is PI3K-Akt signaling pathway, Focal adhesion and Ras signaling pathway. In addition, 34 hub genes were selected by using CytoHubba with degrees >10. Conclusions: Our data reflects that PI3K-Akt signaling pathway, Focal adhesion and Ras signaling pathway may play significant roles in IS, and the hub genes among DEGs(including KDR, ESR1, MMP2, CAV1, PTK2, VWF) may be the potential targets for diagnosis and treatment of IS.