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. Author manuscript; available in PMC: 2017 Dec 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2016 Oct 6;36(12):2358–2368. doi: 10.1161/ATVBAHA.116.307871

Figure 3. AMPK/SIRT1-CTTN regulates eNOS activity.

Figure 3

(A) HUVECs were transfected with control RNA or cortactin siRNA. Transfected cells were kept under static conditions or subjected to PS for 4 hr. Immunoblotting was performed with antibodies as indicated. Data are ratios of p-eNOS 633 to eNOS. (B) HUVECs were transfected with cortactin T401A or T401D plasmid and infected with adenovirus overexpressing SIRT1 (Ad-SIRT1) at 0, 5, and 10 multiplicity of infection (MOI). Data are relative mean ± SEM of NO production, with cells transfected with T401A set to 1. (C) Cortactin+/− MEF cells were transfected with cortactin T401A or T401D plasmid and infected with Ad-SIRT1. (D) HUVECs were transfected with cortactin 9K/Q or 9K/R plasmid and infected with adenovirus overexpressing a constitutive activated form of AMPKα (Ad-AMPK-CA) at 0, 5, and 10 MOI. (E) Cortactin+/− MEFs were transfected with cortactin 9K/Q or 9K/R plasmid and infected with Ad-AMPK-CA. (F, G) HEK293T cells were transfected with cortactin phosphorylation/deacetylation mimic T401D9K/R or dephosphorylation/acetylation mimic T401A9K/Q. Upper panels in A, C, E, and F are immunoblots with indicated antibodies and data are mean ± SEM from 3 independent experiments. eNOS phosphorylation and NO production were assessed in (F) and (G), respectively. ‘*’ indicates P < 0.05.