Atherosclerosis is a leading cause of mortality worldwide. Artery tertiary lymphoid organ (ATLO) neogenesis is affected by abdominal aorta atherosclerosis, which may lead to an immune response. The present study obtained microarray data to investigate the gene expression differences underlying the potential pathogenesis of atherosclerosis and to elucidate the mechanisms underlying ATLO development. Microarray studies of the aorta, plaques, adventitia, blood, spleen, renal lymph nodes and ATLO were downloaded from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) were identified in aorta clusters and ATLO clusters. Kyoto Encyclopedia of Genes and Genomes enrichment and Gene Ontology (GO) analyses were conducted to predict the biological functions of DEGs. The results demonstrated that interleukin 7 receptor (Il7r), C-X-C motif chemokine ligand (Cxcl)16, Cxcl13, Cxcl12, CC motif chemokine receptor 2, CC motif chemokine ligand (Ccl)8, Ccl5 and Ccl12 may function through pathways associated with 'cytokine-cytokine receptor interaction' and 'chemokine signaling pathway' in ATLO. Gene expression alterations were validated by reverse transcription-quantitative polymerase chain reaction. Il7r appeared to be the central gene involved in these events, and chemokines and/or chemokine receptors were visualized by GO enrichment. A protein-protein interaction network was constructed, which suggested that Il7r had a core function in all clusters. Taken together, the results indicated that Il7r upregulation may serve an important role in ATLO development via 'cytokine-cytokine receptor interaction' and 'chemokine signaling pathway'. This may provide novel perspectives for understanding ATLO development and the regulation of the immune response in atherosclerosis.
Vascular calcification (VC) is characterized by calcium phosphate deposition in blood vessel walls and is associated with many diseases, as well as increased cardiovascular morbidity and mortality. However, the molecular mechanisms underlying of VC development and pathogenesis are not fully understood, thus impeding the design of molecular-targeted therapy for VC. Recently, several studies have shown that endoplasmic reticulum (ER) stress can exacerbate VC. The ER is an intracellular membranous organelle involved in the synthesis, folding, maturation, and post-translational modification of secretory and transmembrane proteins. ER stress (ERS) occurs when unfolded/misfolded proteins accumulate after a disturbance in the ER environment. Therefore, downregulation of pathological ERS may attenuate VC. This review summarizes the relationship between ERS and VC, focusing on how ERS regulates the development of VC by promoting osteogenic transformation, inflammation, autophagy, and apoptosis, with particular interest in the molecular mechanisms occurring in various vascular cells. We also discuss, the therapeutic effects of ERS inhibition on the progress of diseases associated with VC are detailed.
S24F is an important component of the chemokine network involved in regulating the biologic activity of RANTES, and its expression can be used in the prevention and treatment of cardiac allograft rejection.
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