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. 2020 Apr 16;40(6):1491–1509. doi: 10.1161/ATVBAHA.120.314252

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© 2020 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 License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited.

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Figure 4. — Galectin-3 antagonizes generation of a proinflammatory macrophage phenotype. LGALS3 (lectin, galactoside-binding, soluble, 3) mRNA expression was silenced for 48 h in human monocyte-derived macrophages, scrambled AllStars oligonucleotides served as a control. A, Quantitative polymerase chain reaction (qPCR) for MMP (matrix metalloproteinase)-1, 2, 8, 10, 11, 12, 14, and 25 mRNA expression; n=4/group; *P<0.05; 2-tailed Student t test. B, Representative Western blot images and relative quantification of MMP12 protein levels in human monocyte-derived macrophages; n=4/group; ***P<0.05; 2-tailed Student t test. Stain-free control is shown as a loading control (LC). Real-time qPCR for TIMP (tissue inhibitor of metalloproteinase) mRNA (C), proinflammatory markers (D), and anti-inflammatory markers (E); n=4/group; *P<0.05 and **P<0.01; 2-tailed Student t test.