Figure 5: Serelaxin Infusion Attenuates Vascular Fibrosis and Fibrotic Gene Expression in the Angiotensin II/L-NG-Nitroarginine Methyl Ester Heart Failure Model

The abdominal aorta was isolated on day 9 (n = 6) or on day 28 (n = 5) of angiotensin II (AngII)/L-NG-nitroarginine methyl ester (L-NAME) infusion. Representative and summary data of aortic medial area from elastin-stained aortas (A) and aortic medial fibrosis from trichrome-stained aortas (B). Black arrows define the tunica media (medial area and degree of fibrosis was measured between arrows). Scale bars represent 1 μm. *p < 0.001; †p < 0.001 for main effects of treatment factor serelaxin versus vehicle; ‡p < 0.001 for main effects of time factor, day 9 versus day 28. (C) Messenger ribonucleic acid was isolated from aortas of mice treated with serelaxin or vehicle, and expression of fibrosis genes was measured by quantitative reverse transcription polymerase chain reaction. *p = 0.018 serelaxin versus vehicle day 9; †p < 0.001, serelaxin day 28 versus vehicle day 28; ‡p = 0.022 for main effects of time factor, day 9 versus day 28; §p < 0.001 for main effects of treatment factor serelaxin versus vehicle; ‖p = 0.049 and ¶p = 0.003, serelaxin day 9 versus serelaxin day 28. Connected single bars over days 9 and 28 indicate analysis of main effects between time points for vehicle and serelaxin in combination. Groups were compared using 2-factor analysis of variance with Tukey post hoc test. Col1 = type 1 collagen; CTGF = connective tissue growth factor; MMP2 = matrix metalloproteinase 2; TGF = transforming growth factor.

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