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. Author manuscript; available in PMC: 2020 Jul 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2019 May 16;39(7):1419–1431. doi: 10.1161/ATVBAHA.118.312346

Figure 5. Sirt1 overexpression prevents nicotine-induced YAP dephosphorylation that mediates arterial extracellular matrix remodeling.

Figure 5.

A. Representative images of IHC staining (left panel) and quantification of YAP (right panel) in aorta from WT and Sirt1-overexpressing (Sirt1Super) mice with or without nicotine treatment (n=5). B. Representative images of IHC staining (left panel) and quantification of pYAP (right panel) in aorta from WT and Sirt1Super mice with or without nicotine treatment (n=5; * P < 0.01 vs. WT/Veh; # P < 0.05 vs. WT/Nic mice). C. YAP knockdown reduced collagen I protein expression (precursor: 140–210KD; mature: 70–90KD) under vehicle and nicotine-treated condition (n=5; * P < 0.01 vs. Con siRNA/Veh; # P < 0.05 vs. Con siRNA/Nic). D. YAP knockdown repressed nicotine-elevated MMP2 protein (n=5; * P < 0.01 vs. Con siRNA/Veh; # P < 0.05 vs. Con siRNA/Nic). Veh, vehicle; Nic, nicotine. Negative controls for staining of anti-YAP and anti-pYAP-S127 were presented in Online Figure IV.