Abstract
Atherosclerosis is one of the most common clinical cardiovascular disorders. Accumulating evidence indicates that lncRNAs exert critical functions in atherosclerosis; however, their functional roles and regulatory mechanisms remain unclear. In this study, we induced atherosclerotic plaques in three rabbit carotid arteries through an atherogenic diet and balloon injury; three age-matched rabbits were fed normal chow and served as controls. We thoroughly investigated the RNA (mRNA, lncRNA and miRNA) expression profiles in atherosclerotic rabbit carotid models with deep RNA sequencing. We identified several significantly differentially expressed RNAs. The corresponding lncRNA-miRNA-mRNA network was constructed, and the significantly dysregulated network was selected. Furthermore, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses indicated that the mRNAs in the network were involved in leukocyte activation, cell proliferation, cell adhesion molecules and cytokine-cytokine receptor interaction. After rigorous screening, we obtained a differentially expressed lncRNA-miRNA-mRNA interaction network associated with atherosclerosis. In the network, XLOC_054118 and XLOC_030217 upregulate the CHI3L1, SOAT, CTSB and CAPG genes by competitively binding to the miRNA ocu-miR-96-5p. XLOC_062719 and XLOC_063297 upregulate CTSS, CTSB and EDNRA genes by competitively binding to the miRNA ocu-miR-185-5p.
Highlights
Atherosclerosis (AS), a chronic disorder affecting the blood vessel walls, is characterized by an imbalance between the inflammatory response and lipid metabolism [1]
We investigated differentially expressed (DE) profiles of miRNA, mRNA and Long noncoding RNAs (lncRNAs) in AS and detected lncRNA-miRNA-mRNA networks in carotid atherosclerotic rabbit models
LncRNAs, miRNAs and mRNAs participate in large-scale competing endogenous RNAs (ceRNAs) crosstalk through MREs
Summary
Atherosclerosis (AS), a chronic disorder affecting the blood vessel walls, is characterized by an imbalance between the inflammatory response and lipid metabolism [1]. AS is the common pathological basis of multiple cardiovascular and cerebrovascular disorders and has become the main cause of mortality and longterm morbidity worldwide [2]. AS medications primarily reduce plasma cholesterol concentrations and blood pressure, effectively reducing tissue damage caused by the disease [3]. Genetic factors represent a major determinant of AS risk [4].
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