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. 2019 Nov 7;40(1):189–205. doi: 10.1161/ATVBAHA.119.313336

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© 2019 The Authors.

Arteriosclerosis, Thrombosis, and Vascular Biology is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

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Figure 9. — Proinflammatory signaling in the aorta. A, Representative images from immunoblotting for P-Stat3 and P-Jnk. B, Quantitative analysis. β-actin served as an internal loading control. WT (wild type) and IL-17KO (IL [interleukin]-17A knockout) mice were treated with (H) and without (N) high salt and β-aminopropionitrile+angiotensin II (B+A). The means (red lines)±SEs (blue lines) are presented for 8 independent experiments in each group. *P<0.05, **P<0.01. N.S. indicates not significant.