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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 produced a harmful change in the targeted oxidative stress–, inflammation‐, and proteolysis‐related gene expressions in the carotid arteries of cathepsin S wild‐type (CatS^+/+) mice. A through F, Quantitative polymerase chain reaction data show the levels of p22^phox, p47^phox, p67^phox, nicotinamide‐adenine dinucleotide phosphate, reduced form, oxidase 1 (NOX‐1), gp91^phox, intercellular adhesion molecule‐1 (ICAM‐1), vascular cell adhesion molecule‐1 (VCAM‐1), monocyte chemoattractant protein‐1 (MCP‐1), stromal cell–derived factor‐1α (SDF‐1α), C‐X‐C chemokine receptor‐4 (CXCR‐4), toll‐like receptor (TLR)‐2, TLR‐4, tumor necrosis factor‐α (TNF‐α), interleukin‐1β (IL‐1β), angiotensin II receptor 1α (ATR1α), matrix metalloproteinase (MMP)‐9, MMP‐2, cathepsin L (CatL), and CatS mRNAs. Results are mean±SEM (n=5–7). ***P<0.001 vs nonstressed group by 1‐way ANOVA, followed by Tukey post hoc tests.