Resolution of Inflammation Through the Lipoxin and ALX/FPR2 Receptor Pathway Protects Against Abdominal Aortic Aneurysms
Marcelo H. Petri, Silke Thul, Teodora Andonova, Moritz Lindquist-Liljeqvist, Hong Jin, Nikolaos-Taxiarchis Skenteris, Hildur Arnardottir, Lars Maegdefessel, Kenneth Caidahl, Mauro Perretti, Joy Roy and Magnus Bäck
Fpr2 and LO Deficiencies Exacerbate Ang II-induced Aortic Dilation
(A) Aortic dimensions in ApoE−/−×Fpr2+/+(circles) and ApoE−/−×Fpr2−/−(squares) mice, implanted with osmotic pumps containing Ang II (1 μg/kg/min). (Left) Ultrasonography measurements of the inner edges of the suprarenal abdominal aorta before implantation (Base) and every week until sacrifice (4 weeks). (Right) Echocardiographic images at week 4. (B) Ex-vivo measurements of aortic dilation from the outer edges of the abdominal segments. (Right) Representative images of each genotype. (C) Ultrasonographic measurements of aortic dimensions in a second series of ApoE−/−×Fpr2+/+(circles), ApoE−/−×Fpr2−/−(squares), and ApoE−/−×12/15LO−/−(triangles) mice treated with Ang II (1 μg/kg/min). Ultrasonography measurements of the inner edges of the suprarenal abdominal aorta before implantation (Base) and every 2 weeks until sacrifice (4 weeks). Representative echocardiographic images show measurements by genotype at week 4. At least n = 6 in each group and graphs represent mean ± SEM. *p < 0.05 of ApoE−/−×Fpr2+/+ versus ApoE−/−×Fpr2−/−; #p < 0.05 of ApoE−/−×Fpr2+/+ and ApoE−/−×12/15LO−/−. Ang II = angiotensin II; ApoE = apolipoprotein E; LO = 12/15-lipoxygenase.