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Identification and functional analysis of differentially expressed genes associated with cerebral ischemia/reperfusion injury through bioinformatics methods.

ABSTRACT: Cerebral ischemia/reperfusion (I/R) injury results in detrimental complications. However, little is known about the underlying molecular mechanisms involved in the reperfusion stage. The aim of the present study was to identify a gene expression profile associated with cerebral ischemia/reperfusion injury. The GSE23160 dataset, which comprised data from sham control samples and post?I/R injury brain tissues that were obtained using a middle cerebral artery occlusion (MCAO) model at 2, 8 and 24 h post?reperfusion, was downloaded from the Gene Expression Omnibus database. The differentially expressed genes (DEGs) in the MCAO samples compared with controls were screened using the GEO2R web tool. Gene Ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis for DEGs was performed using the online tool DAVID. Furthermore, a protein?protein interaction (PPI) network was constructed using the STRING database and Cytoscape software. In total, 32 DEGs at 2 h post?reperfusion, 39 DEGs at 8 h post?reperfusion and 91 DEGs at 24 h post?reperfusion were identified, while 15 DEGs were common among all three groups. GO analysis revealed that the DEGs at all three time?points were enriched in 'chemotaxis' and 'inflammatory response' terms, while KEGG pathway analysis demonstrated that DEGs were significantly enriched in the 'chemokine signaling pathway'. Furthermore, following PPI network construction, Cxcl1 was identified as the only hub gene that was common among all three time?points. In conclusion, the present study has demonstrated a global view of the potential molecular differences following cerebral I/R injury and may contribute to an improved understanding of the reperfusion stage, which may ultimately aid in the development of future clinical strategies.

SUBMITTER: Shao X

PROVIDER: S-EPMC6072188 | biostudies-literature | 2018 Aug

REPOSITORIES: biostudies-literature

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Identification and functional analysis of differentially expressed genes associated with cerebral ischemia/reperfusion injury through bioinformatics methods.

Shao Xiaoli X Bao Wangxiao W Hong Xiaoqin X Jiang Huihua H Yu Zhi Z

Molecular medicine reports 20180606 2

Cerebral ischemia/reperfusion (I/R) injury results in detrimental complications. However, little is known about the underlying molecular mechanisms involved in the reperfusion stage. The aim of the present study was to identify a gene expression profile associated with cerebral ischemia/reperfusion injury. The GSE23160 dataset, which comprised data from sham control samples and post‑I/R injury brain tissues that were obtained using a middle cerebral artery occlusion (MCAO) model at 2, 8 and 24 h ...[more]

PMID: 29901134

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Project description:BACKGROUND:Ischemic stroke is a deadly disease that poses a serious threat to human life. Superoxide dismutase 3 (SOD3, ECSOD) is the main antioxidant enzyme that removes superoxide anions from cells. This study aimed to investigate the effect of SOD3 overexpression on cerebral ischemia-reperfusion injury in rats. METHODS:GV230-EGFP-ECSOD, the recombinant SOD3-overexpressed vector, was constructed by genetic engineering technology, and mesenchymal stem cells (MSCs) were infected with lentiviral packaging. In animal experiment, cerebral ischemia-reperfusion injury model rats were successfully established. ECSOD-MSCs are the MSCs that successfully transfected with SOD3 overexpression vector. The animals were injected with ECSOD-MSCs (ECSOD-MSC group), normal MSCs (MSCs group), PBS (PBS group), and not do any processing (Model group) via the tail vein. Then MRI was used to detect the infarct volume of rats, modified Neurological Severity Scores (mNSS), and immunohistochemistry were used to evaluate the expression of neurological function and apoptosis-related genes in rats. RESULTS:Western blot analysis revealed that the SOD3 was highly expressed in MSCs. Animal experiments showed that the transplantation of ECSOD-MSCs significantly reduced the infarct volume of ischemic stroke rats (p < 0.05), significantly improved neurological function in rats (p < 0.05), and found proapoptotic gene, Bax, expression was significantly decreased (p < 0.05), the expression of anti-apoptotic gene, Bcl-2, was significantly increased (p < 0.05). The highly expressed SOD3 has no correction with brain infarct volume, and the highly expressed SOD3 has a positive correlation with cell apoptosis. It is speculated that overexpression of SOD3 affects the expression of Bax and Bcl-2, and improves apoptosis to alleviate ischemic stroke. CONCLUSION:Our results indicated that MSCs transfected with SOD3 can effectively alleviate cerebral ischemia-reperfusion injury in rats.

Dataset Information

Identification and functional analysis of differentially expressed genes associated with cerebral ischemia/reperfusion injury through bioinformatics methods.

Publications

Identification and functional analysis of differentially expressed genes associated with cerebral ischemia/reperfusion injury through bioinformatics methods.

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