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. 2019 Jul 12;8(14):e011994. doi: 10.1161/JAHA.119.011994

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© 2019 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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Stress accelerated the oxidative stress production and macrophage infiltration in response to injury at day 4. A and B, Representative images of dihydroethidium staining and quantitative data for positive staining area of the injured arterial tissues. C and D, Representative images and quantitative data for CD68⁺ cell numbers (arrowheads). E through G, Representative images of gelatin zymography and combined quantitative data for gelatinolytic activities of matrix metalloproteinase (MMP)‐2 and MMP‐9 in the nonstressed and stressed groups. Bar=100 μm. Results are mean±SEM (n=4–6). CatS^+/+ indicates cathepsin S wild type; NS, no significance. ***P<0.001 vs nonstressed group by 1‐way ANOVA, followed by Tukey post hoc tests.