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. 2022 Feb 24;42(4):428–443. doi: 10.1161/ATVBAHA.121.317365

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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 License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited.

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Figure 4. — Downregulation of genes involved in vascular smooth muscle differentiation and contraction in Y/T KO (YAP/TAZ [yes-associated protein 1/WW domain containing transcription regulator 1] knockout) mice. RNA sequencing was performed on aortae from Ctrl (control) and Y/T KO mice. A, Protein Analysis Through Evolutionary Relationships (PANTHER) overrepresentation test and PANTHER GO-slim cellular component of significantly downregulated genes with fold enrichment in black and false discovery rate in red. B, Confirmation of selected smooth muscle markers by RT-qPCR (Ctrl, n=5–6; Y/T KO, n=5–6). C, Quantification of Western blot analysis of SM-MHC (smooth muscle α-actin and myosin heavy chain) and their representative blots to the right. Targets were normalized to the total protein (Ctrl, n=6–9; Y/T KO, n=6–9). D, Reverse transcription-quantitative polymerase chain reaction analysis of Myocd, Rock1, Avpr1, and Htr2a mRNA expression (Ctrl, n=5–6; Y/T KO, n=6). E, Western blot analysis of ROCK1 (Rho kinase 1; Ctrl, n=6; Y/T KO, n=6). All data are presented as mean±SEM. FC indicates fold change; FDR, false discovery rate; and KO, knockout.