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. 2020 May 7;9(10):e014761. doi: 10.1161/JAHA.119.014761

Figure 1. Local application of leptin antagonist (LepA) inhibits medial degeneration.

Figure 1

Histological characterization of aortic root wall in Marfan syndrome (MFS) mice (30 days postoperatively for MFS and LepA‐treated MFS mice, 11 weeks for all). (A1‐3) Verhoeff–van Gieson (VVG) staining in MFS, LepA‐treated MFS mice, and untreated wild‐type (WT) mice. Note multiple disruptions of medial elastic fibers in MFS vs preserved elastic lamellae in LepA‐treated MFS mouse, which was comparable to WT. (B1‐3) Masson trichrome staining demonstrating depletion of smooth muscle cells and increased deposition of extracellular collagenous material in MFS (arrows) compared with LepA‐treated MFS and WT untreated mice. Bars=50 μm (A and B). C, Number of fractures in medial elastic fibers per viewed field in aortic root from MFS, LepA‐treated MFS, and WT mice. D, Wall thickness of aortic root from MFS, LepA‐treated MFS, and WT mice. (E1, 2) Immunohistochemistry analysis for Mac2 in MFS and LepA‐treated MFS mice. There is macrophage infiltration in the aortic root media of the MFS (white arrows), whereas the LepA‐treated MFS aortic root media are devoid of inflammatory cells, with macrophages only in the perivascular tissue (black arrows). The white broken line defines the medial border. **P<0.01, *** P<0.001. (F1‐4) Matrix metalloproteinase 9 (MMP9) antigen was abundantly demonstrated within aortic wall and periaortic inflammatory infiltrates in MFS (1), higher magnification (2), absent in WT mice (3), and rarely evident in LepA‐treated MFS mice (4).