Abstract
Ischemia/reperfusion (I/R) refers to situations where blood is perfused into ischemic or hypoxic tissues, potentially resulting in an inflammatory response and oxidative injury. This study was conducted to explore the pathogenesis of I/R injury. GSE82146 was extracted from the Gene Expression Omnibus, consisting of 15 complete global brain ischemia (CGBI) reperfusion hippocampus samples and 12 non-ischemic control (NIC) hippocampus samples. The differentially expressed genes (DEGs) between the CGBI and NIC samples were selected using LIMMA package, and were then analyzed with weighted gene co-expression network analysis (WGCNA). Using DAVID software, the DEGs in significant modules were run through enrichment analysis. The DEGs in significant modules were merged, and then a protein-protein interaction (PPI) network was built for them using Cytoscape software. After miRNAs and transcription factors (TFs) were predicted for the DEGs using the WebGestalt tool, a TF-miRNA-target regulatory network was built using Cytoscape software. Furthermore, quantitative real-time polymerase chain reaction (qRT-PCR) analysis was conducted to detect the levels of key genes. There were 390 DEGs in the CGBI samples. Based on WGCNA, brown and turquoise modules were screened as CGBI-associated modules. In the PPI network, key nodes HSP90AA1 and HSPA5 were able to interact with each other. In the regulatory network, MYC, HSF1 and miR-22 had higher degree values. Moreover, HSPA5 was targeted by MYC in the regulatory network. In addition, upregulated HSPB1 and HMOX1, as well as downregulated NR4A2, were confirmed with qRT-PCR analysis. HSPB1, HMOX1 and NR4A2 were the key genes correlated with I/R injury. Additionally, HSP90AA1, HSPA5, MYC, HSF1, and miR-22 might be related to the pathogenesis of I/R injury.
Highlights
Ischemia/reperfusion (I/R) refers to a situation where blood is perfused into tissues experiencing ischemia or hypoxia.[1]
HSP90AA1, HSPA5, myelocytomatosis oncogene (MYC), heat shock transcription factor 1 (HSF1), and miR-22 might be related to the pathogenesis of I/R injury
Ischemia/reperfusion is usually related to microvascular injury, and the imbalance of reactive oxygen species (ROS) and nitric oxide (NO) produced by activated endothelial cells is responsible for the subsequent inflammatory response.[3,4]
Summary
Ischemia/reperfusion (I/R) refers to a situation where blood is perfused into tissues experiencing ischemia or hypoxia.[1]. I/R promotes the repair of damage and the recovery of functioning in most cases, it can lead to an inflammatory response and oxidative injury by inducing oxidative stress.[2]. Ischemia/reperfusion is usually related to microvascular injury, and the imbalance of reactive oxygen species (ROS) and nitric oxide (NO) produced by activated endothelial cells is responsible for the subsequent inflammatory response.[3,4]. The development of I/R injury is influenced by ischemia time, aerobic degree, collateral circulation, and reperfusion conditions. The I/R injury has a powerful influence on the ischemic cascade of the brain, involving brain trauma and stroke.[5]. Ischemia/reperfusion (I/R) refers to situations where blood is perfused into ischemic or hypoxic tissues, potentially resulting in an inflammatory response and oxidative injury
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