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. 2020 Jul 30;127(8):997–1022. doi: 10.1161/CIRCRESAHA.120.317295

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© 2020 The Authors.

Circulation Research 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 6. — Depletion of basement-membrane proteins in ruptured human carotid plaques and in aortas of SR-uPA^+/0 mice.

A, Data from 2 sets of human carotid plaques. Shotgun proteomics was performed on stable (open bars) and ruptured (shaded bars) segments of 2 independent sets of plaques (1 and 2). Analyses were performed independently, 1 y apart. Proteins were selected for this analysis based on their significantly decreased abundance in the first set of human plaques and—for basement-membrane proteins—congruently decreased abundance in SR-uPA^+/0 mouse aortas. B, Data from aortas of 20-week-old SR-uPA^+/0 and SR-uPA^0/0 mice. A and B, Individual data points (n=6 per group) indicate individual plaque segments (A) or aortas (B); group medians and interquartile ranges are shown. PSM indicates peptide-spectrum match. P: #<0.1, *<0.05, **<0.01, and ***<0.005.