Ischemic stroke is a leading cause of mortality and permanent disability, with enormous financial repercussions on health systems worldwide. Ischemic brain injury results from a complex sequence of pathophysiological events that evolve over time. In order to examine the molecular mechanisms underlying middle cerebral artery occlusion (MCAO)-induced ischemic stroke, the GSE35338 affymetrix microarray data was obtained from the Gene Expression Omnibus database and the differentially expressed genes (DEGs) between samples from patients with MCAO-induced ischemic stroke and sham controls at various time points were identified. Furthermore, protein-protein interaction (PPI) networks were constructed by mapping the DEGs into PPI data to identify the pathways that these DEGS are involved in. The results revealed that the expression of 438 DEGs, which are mainly involved in cell death, oxidant reduction, cell cycle and cell-cell signaling, were altered in MCAO samples. The nodes of CXC motif chemokine 10 (CXCL10) and interleukin-6 (IL-6) were large, with degrees of >20. In conclusion, the results suggest that CXCL10 and IL-6 have important roles in the occurrence and progression of MCAO-induced ischemic stroke.

ABSTRACT. We investigated the effects of type 1 diabetes mellitus (T1DM) on endothelial progenitor cells (EPCs) at the molecular level and assessed the therapeutic potential of folic acid (FA) in DM. We downloaded the gene expression profile of the EPCs from T1DM patients before and after treatment with FA and from healthy controls. We identified the differentially expressed genes (DEGs) in the EPCs from T1DM patients before and after a four-week period of FA treatment and compared them with those obtained from the healthy subjects by using limma package in R language. Then, functional annotation of the DEGs was performed using the online tool Database for Annotation, Visualization and Integrated Discovery (DAVID) based on the Kyoto Encyclopedia of Genes and Genomes database. The expression of 696 genes was altered in the EPCs from T1DM patients compared to those from the healthy controls. These genes were mainly involved in the pathways associated with immune response. FA can normalize majority of the altered gene expression profiles of EPCs from T1DM patients to resemble those of healthy subjects, albeit with some side effects. FA can be a potential therapeutic agent for the treatment of T1DM. However, focused efforts are required to ensure that the dose of FA falls within the permissible pharmacological range.