MEDICAL SCIENCES Correction for “Cyclooxygenase-1, not cyclooxygenase-2, is responsible for physiological production of prostacyclin in the cardiovascular system,” by Nicholas S. Kirkby, Martina H. Lundberg, Louise S. Harrington, Philip D. M. Leadbeater, Ginger L. Milne, Claire M. F. Potter, Malak Al-Yamani, Oladipupo Adeyemi, Timothy D. Warner, and Jane A. Mitchell, which appeared in issue 43, October 23, 2012, of Proc Natl Acad Sci USA (109:17597–17602; first published October 8, 2012; 10.1073/pnas.1209192109).
The authors note that Fig. 6 appeared incorrectly. The corrected figure and its legend appear below. This error does not affect the conclusions of the article.
Fig. 6.
Role of COX-1 versus COX-2 in driving prostacyclin production in the circulation in vivo. (A) Prostacyclin release in vivo was measured as 6-ketoPGF1α levels in plasma under control (basal) conditions and after administration of bradykinin (100 nmol/kg; i.v.) in wild-type, COX-1−/−, and COX-2−/− mice (n = 6). COX inhibitory activity of blood from mice treated with i.v. parecoxib (0.5 mg/kg), diclofenac (1 mg/kg), or vehicle was measured ex vivo (B) in A23187-stimulated whole blood for COX-1 or (C) on LPS-induced murine J774 macrophages for COX-2 (n = 4). The effect of the parecoxib and diclofenac on prostacyclin release in vivo in wild-type mice was measured as 6-ketoPGF1α levels in plasma under (D) control (basal) conditions and (E) after administration of bradykinin (100 nmol/kg; i.v.). Data are mean ± SEM for n = 6 male and female, 10- to 12-wk-old mice per genotype. Data were analyzed using one-way ANOVA followed by Bonferroni’s multiple comparison test; *P < 0.05 vs. wild type.