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. 2022 Jun 16;42(8):1005–1022. doi: 10.1161/ATVBAHA.121.317451

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© 2022 The Authors.

Arteriosclerosis, Thrombosis, and Vascular Biology is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

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Figure 2. — Single-cell transcriptomics of Perk^SMC−/− and Perk^SMC+/+ aortas at baseline and after hypercholesterolemia show loss of a specific subset of modulated smooth muscle cells (SMCs) in the Perk^SMC−/− aortas. A, Modulated SMC clusters mSMC1 and mSMC2 expanded and appeared in the hypercholesterolemic Perk^SMC+/+ mice with plaque formation, but mSMC2 did not appear in the Perk^SMC−/− aortas with hypercholesterolemia. B, Perk deletion rescues the loss of contractile SMCs in Perk^SMC+/+ aortas following HFD (top). mSMC1 cells are present at baseline in both genotypes and increase to a similar level following hypercholesterolemia. However, mSMC2 cells are rare at baseline in both mice but expand dramatically in Perk^SMC+/+ aortas compared with Perk^SMC−/− aortas. C, Expression patterns of contractile and SMC modulation markers in Perk^SMC+/+ aortas following hypercholesterolemia. D, Top pathways in which DEGs of mSMC and cSMC clusters are enriched. E, Correlation plot indicates that mSMC1 and mSMC2 cells highly correlate with each other, as well as with contractile SMCs. Data are represented as mean±SD.