Macrophage extracellular traps originated from the vascular smooth muscle cells play key roles in atherosclerosis progression [scRNA-seq]

Smooth muscle cells (SMC) play significant roles in atherosclerosis via phenotypic switching, a pathological process in which SMC transdifferentiation into macrophage-like SMCs. Furthermore, during transdifferentiation, the SMCs' expression of PADI4 upregulating and SMC generated extracellular trap, a web-like structure, which plays key role in the development of atherosclerosis plaque. To reveal the function of SMC's generating ETs during atherosclerosis and to identify molecular targets for disease therapy, we combined SMC fate mapping and single-cell RNA sequencing of mouse atherosclerotic plaques. Overall design: SMC-lineage tracing mice, B6-G/R; Myh11-CreERT2;Padi4(flox/flox) mice, were crossed onto B6-G/R Myh11cre group as control group and B6-G/R Myh11cre Padi4flox/flox group as case group to specific knock out the Padi4 within SMC. Mouse single cells digested from arterial tissues (including ascending aorta, brachiocephalic artery and thoracic aorta) for scRNA-seq were prepared from six mice of each group at the same timepoint of Western diet (WD) feeding (26 weeks). Alive tdTomato+ cells (SMC-lineage cells) and ZsGreen cells (none-SMC linage cells) were sorted separately and were immediately subjected to scRNA-seq using Chromium Single Cell Gene Expression system (10x Genomics) in parallel.