RNA-seq in aortic smooth muscle cells from a mice lacking Arg1 expression in erytrhrocytes (RBC.ARG1-KO) and their litter mate controls (RBC.ARG1-WT) after culture in standard DMEM or foam cell medium (DIAM)

Endothelial dysfunction is an early event in atherosclerosis development and centrally linked with insufficient endothelial nitric oxide (NO) production. However, supraphysiological chronically increased NO levels, including from other cellular sources, also may induce endothelial dysfunction, and may play a role. Here, we studied how chronically elevated NO production from erythrocytes, achieved by genetic deletion of arginase-1 (ARG1), impacts smooth muscle cell (SMC) lipid accumulation and atherosclerosis progression.