Key result
Rat pulmonary embolism alters ~346 genes at 18 hours, highlighting chemokine and inflammatory signaling.
Why the study?
The functional roles and interactions of differentially expressed genes in pulmonary embolism remain to be explored.
Bioinformatics analysis identified key differentially expressed genes (such as TFPI2 and TNF) and pathways (chemokine, inflammatory, immune) that may serve as potential therapeutic targets for pulmonary embolism.
Answers are grounded in this paper and cite their sources.
Provides candidate targets for PE research; leaves open translation to care without validation.
The aim of the present study was to explore the function and interaction of differentially expressed genes (DEGs) in pulmonary embolism (PE). The gene expression profile GSE13535, was downloaded from the Gene Expression Omnibus database. The DEGs 2 and 18 h post‑PE initiation were identified using the affy package in R software. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways of the DEGs were analyzed using Database for Annotation Visualization and Integrated Discovery (DAVID) online analytical tools. In addition, protein‑protein interaction (PPI) networks of the DEGs were constructed using the Search Tool for the Retrieval of Interacting Genes/Proteins. The PPI network at 18 h was modularized using Clusterone, and a functional enrichment analysis of the DEGs in the top three modules was performed with DAVID. Overall, 80 and 346 DEGs were identified 2 and 18 h after PE initiation, respectively. The KEGG pathways, including chemokine signaling and toll‑like receptor signaling, were shown to be significantly enriched. The five highest degree nodes in the PPI networks at 2 or 18 h were screened. The module analysis of the PPI network at 18 h revealed 11 hub nodes. A Gene Ontology terms analysis demonstrated that the DEGs in the top three modules were associated with the inflammatory, defense and immune responses. The results of the present study suggest that the DEGs identified, including chemokine‑related genes TFPI2 and TNF, may be potential target genes for the treatment of PE. The chemokine signaling pathway, inflammatory response and immune response were explored, and it may be suggested that these pathways have important roles in PE.
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Wang et al. (2014) studied Pulmonary embolism (n=22). Microsphere injection (PE model) vs. Vehicle injection was evaluated on Number of differentially expressed genes (DEGs). Microsphere-induced pulmonary embolism in rats resulted in 80 and 346 differentially expressed genes at 2 and 18 hours, respectively, highlighting the potential role of chemokine signaling and inflammatory responses.
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