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. 2020 May 14;40(7):1722–1737. doi: 10.1161/ATVBAHA.120.314370

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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 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 2. — Adeno-associated viral (AAV)-sVEGFR3 (soluble vascular endothelial growth factor receptor 3) therapy inhibits infarct lymphangiogenesis postmyocardial infarction (MI). Mice were treated with AAV-hVEGF (human VEGF)-C_C156S gene therapy (red circles, n=8), sVEGFR3 (AAV-sVEGFR3, blue triangles, n=5–7), or AAV-scrambled virus (MI controls, black circles, n=8), and sham-operated mice (white circle, n=7–9) served as healthy controls. Lymphangiogenesis in the infarct scar was evaluated as % proliferating lymphatic vessels (A), open lymphatic densities (B), and lymphatic area at 7 or 21 days post-MI (C). Examples (D) at 21 days post-MI of infarct zone left ventricular lymphatics (Lyve1 [lymphatic vessel endothelial receptor 1], red), macrophages (F4-80, gray), and cell nuclei (DAPI, blue); ×20 magnification, scale bar=50 µm. Note LYVE1-expressing macrophages close to lymphatic vessels. con indicates control.