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. Author manuscript; available in PMC: 2011 Oct 1.
Published in final edited form as: Circ Res. 2010 Aug 12;107(7):877–887. doi: 10.1161/CIRCRESAHA.110.222968

Figure 1.

Figure 1

Figure 1

Low concentrations of aspirin rapidly acetylate eNOS on lysine residues and stimulate eNOS enzymatic activity and NO production. A to C, Micromolar concentrations of aspirin rapidly stimulate lysine acetylation of eNOS. Representative immunoblots for acetylated lysine (Ac-Lys, Ac-K) in eNOS immunoprecipitated (from A to B) HEK 293 cells expressing ectopic eNOS and (C) HUVEC showing dose- and time-response to aspirin (ASA). Accompanying graphs show analysis by densitometry of Ac-K/total eNOS relative to no aspirin from independent blots. D to E, Low concentrations of aspirin increase NO metabolites (nitrite + nitrate) in conditioned media of (D) HEK 293 cells expressing ectopic eNOS and (E) HUVEC. F, Low concentrations of aspirin increase enzymatic activity (conversion of arginine to citrulline) of eNOS ectopically expressed in HEK 293 cells. (G) Knockdown of COX-1 does not suppress aspirin-stimulated NO (nitrite + nitrate) in conditioned media of HUVEC. *P<0.05 and **P< 0.01 (n=3 to 4).