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. 2020 Jul 16;9(14):e016134. doi: 10.1161/JAHA.120.016134

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© 2020 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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Bio‐functional testing corroborates high‐HMGB1 (high mobility group box 1) and low‐LAMC1 (laminin gamma chain 1) expression in abnormal subjects (A) vs normal subjects (N). Left, HMGB1 content of culture medium over blood outgrowth endothelial cells measured ± lipopolysaccharide stimulation for 24 hours. Baseline release (white bars) tended to be higher for abnormal vs normal subjects (P=0.158). In response to lipopolysaccharide (black bars), abnormal blood outgrowth endothelial cells released 13.3‐fold greater HMGB1 (P=8.5×10⁻⁵). The specific subjects studied are indicated in red in the embedded HMGB1 expression plot. Right, LAMC1 deposition into collagen subendothelial matrix by abnormal blood outgrowth endothelial cells over 14 days incubation was, on average, one tenth that by normal blood outgrowth endothelial cells. LPS indicates lipopolysaccharide.