Abstract
Cell-cell communication coordinates cellular differentiation, tissue homeostasis, and immune responses in states of health and disease. In abdominal aortic aneurysm (AAA), a relatively common and potentially life-threatening vascular disease, intercellular communications between multiple cell types are not fully understood. In this study, we analyzed published single-cell RNA sequencing (scRNA-seq) datasets generated from the murine CaCl2 model, perivascular elastase model, Angiotensin II model, and human AAA using bioinformatic approaches. We inferred the intercellular communication network in each experimental AAA model and human AAA and predicted commonly altered signaling pathways, paying particular attention to thrombospondin (THBS) signaling between different cell populations. Together, our analysis inferred intercellular signaling in AAA based on single-cell transcriptomics. This work provides important insight into cell-cell communications in AAA and has laid the groundwork for future experimental investigations that can elucidate the cell signaling pathways driving AAA.
Highlights
Abdominal aortic aneurysm (AAA), defined as a focal dilation of the abdominal aorta beyond 50% of its normal diameter, is a common and potentially lethal aortic disease [1]
Cells were clustered into 12 populations, including two fibroblast (Fib), two smooth muscle cell (SMC), and three macrophage (Maph) populations, as well as several other cell types such as endothelial cell (EC), neutrophil (Neutro), dendritic cell (DC), T and natural killer cell (T/NK), and B cell (Supplementary Figure 1A)
Cell-cell communication plays a fundamental role in governing tissue function, regulating individual cell processes, and intercellular relationships, driving tissue homeostasis and pathophysiology in states of health and disease [12, 13]
Summary
Abdominal aortic aneurysm (AAA), defined as a focal dilation of the abdominal aorta beyond 50% of its normal diameter, is a common and potentially lethal aortic disease [1]. Experimental data implicate the importance of intercellular communication between inflammatory cells and SMCs during aneurysm development [3]. Various anti-inflammatory strategies that were found to prevent aneurysm formation in mice were shown to reduce SMC death and preserve the contractile phenotype in the aortic wall [4, 5]. Inhibiting cell death in aneurysm models has been shown to reduce intra-aortic accumulation of inflammatory cells [6, 7]. Despite these early insights, a comprehensive understanding of communication patterns between different cell populations in healthy and aneurysmal aorta remains elusive
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