Bioinformatics Analysis Reveals Cell Cycle-Related Gene Upregulation in Ascending Aortic Tissues From Murine Models.

Tao Qiu,Xuxia Liu,Xiaoyan Li,Qingle Li,Tongxun Li,Yueli Wang,Xiaoping Zhang,Xipeng Wang,Zuozhen Yang

doi:10.3389/fgene.2022.823769

Abstract

Thoracic aortic aneurysm and dissection (TAAD) is a high-risk aortic disease. Mouse models are usually used to explore the pathological progression of TAAD. In our studies, we performed bioinformatics analysis on a microarray dataset (GSE36778) and verified experiments to define the integrated hub genes of TAAD in three different mouse models. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) and protein–protein interaction (PPI) network analyses, and histological and quantitative reverse transcription-PCR (qRT–PCR) experiments were used in our study. First, differentially expressed genes (DEGs) were identified, and twelve common differentially expressed genes were found. Second, genes related to the cell cycle and inflammation were enriched by using GO and PPI. We focused on filtering and validating eighteen hub genes that were upregulated. Then, expression data from human ascending aortic tissues in the GSE153434 dataset were also used to verify our findings. These results indicated that cell cycle-related genes participate in the pathological mechanism of TAAD and provide new insight into the molecular mechanisms of TAAD.

Highlights

Thoracic aortic aneurysm and dissection (TAAD) is a surgical emergency
Many mouse models have been used in mechanistic studies, such as Fbn1 C1039G/+ mice
Expressed genes (DEGs) of three TAAD mice model comparison with CON was analyzed by GEO2R online tools, the R package was used for DGE identification, the data was transformed by log2 and the Benjamini & Hochberg (False discovery rate) was applied adjustment to the p-values

Summary

Introduction

Thoracic aortic aneurysm and dissection (TAAD) is a surgical emergency. The onset of TAAD is usually sudden, without warning. Risk factors for TAAD include age, sex, hypertension, hypercholesterolemia, smoking and connective tissue disorders (Gawinecka, et al, 2017; Nienaber and Clough, 2015). Diagnostic and therapeutic techniques for TAAD have improved; its overall mortality remains high (Evangelista, et al, 2018; Melvinsdottir, et al, 2016). Research on the molecular mechanisms and pathological progression of TAAD is crucial. Many mouse models have been used in mechanistic studies, such as Fbn C1039G/+ mice

Methods

Results

Conclusion