Venous thromboembolism (VTE) is a common vascular disease and a major cause of mortality. This study intended to explore the biomarkers associated with VTE by bioinformatics analyses.Based on Gene Expression Omnibus (GEO) database, the GSE19151 expression profile data were downloaded. The differentially expressed genes (DEGs) between single VTE (sVTE)/recurrent VTE (rVTE) and control were identified. Then, pathway enrichment analysis of DEGs were performed, followed by protein–protein interaction (PPI) network construction.Total 433 upregulated and 222 downregulated DEGs were obtained between sVTE and control samples. For rVTE versus control, 625 upregulated and 302 downregulated DEGs were identified. The overlap DEGs were mainly enriched in the pathways related to ribosome, cancer, and immune disease. The DEGs specific to rVTE were enriched in several pathways, such as nod-like receptor signaling pathway. In the PPI network, 2 clusters of VTE genes, including ribosomal protein family genes and NADH family-ubiquinol-cytochrome genes, were identified, such as ribosomal protein L9 (RPL9), RPL5, RPS20, RPL23, and tumor protein p53 (TP53).The nod-like receptor signaling pathway, ribosomal protein family genes, such as RPL9, RPL5, RPS20, and RPL23, and DEG of TP53 may have the potential to be used as targets for diagnosis and treatment of VTE.
Atherosclerosis (AS) is the main cause of morbidity and mortality in the world. Mitochondrial dysfunction is closely related to AS. At present, several signaling pathways related to mitochondrial dysfunction have been found, one of which is around PGC-1α. PGC-1α is a transcription activator, which is related to mitochondrial biogenesis and antioxidant defense. In this study, we explored the effect of miR-18a-5p/PGC-1α signaling pathway on mitochondrial energy metabolism in HAECs with ox-LDL treatment. The results showed that the mitochondrial energy metabolism disorder in HAECs treated by ox-LDL was related to the downregulation of LncRNA FENDRR and PGC-1α. FENDRR could reverse ox-LDL induced mitochondrial energy metabolism disorder and upregulate the PGC-1α expression. FENDRR could be used as ceRNA to inhibit the miR-18a-5p expression and reduce the negative regulation of miR-18a-5p on PGC-1α. Downregulation of miR-18a-5p expression or upregulation of PGC-1α in ox-LDL treated HAECs could reverse mitochondrial energy metabolism disorder. In conclusion, these findings suggested that FENDRR/miR-18a-5p/PGC-1α signaling pathway regulated mitochondrial energy metabolism in HAECs; ox-LDL downregulated the expression of PGC-1α and cause mitochondrial energy metabolism disorder by inhibiting this signal pathway.
The present study aimed to investigate potential gene markers for predicting the formation of carotid atheroma plaques using high-throughput bioinformatics methods. The GSE43292 gene expression profile was downloaded from the Gene Expression Omnibus database. Following data processing, differentially expressed genes (DEGs) were screened using a paired t-test in the Linear Models for Microarray Data package with the criteria of a false discovery rate of P<0.05 and |log2 fold-change| ≥0.58, followed by functional enrichment, protein-protein interaction (PPI) network construction, key node and module analysis, and prediction of transcription factors (TFs) targeting genes in the significant modules. The results revealed that the gene expression profiles from 32 paired samples of carotid atheroma plaque tissue and macroscopically intact tissue were obtained, based on which 886 DEGs, including 513 upregulated genes and 373 downregulated genes, were identified. The upregulated and downregulated gene sets were enriched in 24 and 13 pathways, respectively. The PPI network constructed with these DEGs comprised 35 key nodes with degrees ≥20, among which spleen tyrosine kinase (SYK), LYN and phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit γ (PIK3CG) were the three highest. A significant module was mined in the PPI network, which consisted of 29 DEGs targeted by 11 TFs. The DEGs between the carotid atheroma plaque and macroscopically intact tissue samples may be involved in carotid atherogenesis. Key nodes in the PPI network constructed from these DEGs and the genes involved in the significant module, including SYK, LYN and PIK3CG, are promising for the prediction of carotid plaque formation.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.