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. 2021 Jul 21;218(8):e20200938. doi: 10.1084/jem.20200938

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© 2021 Hisata et al.

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Figure 7. — Loss of EC LRG1 blocks the development of emphysema in the murine elastase model. (A) Schematic of generation of mouse line with EC-specific loss of Lrg1 expression. Transgenic mice in which VE-cadherin promoter drives expression of tamoxifen-responsive Cre^ERT2 (VE-Cad–Cre^ERT2 mice) were crossed with Lrg1^loxP^/loxP mice and treated with tamoxifen to induce EC-specific deletion of LRG1. (B) Representative immunofluorescent images of lung sections stained for LRG1 (red), DAPI (blue), SPC (green, middle panel), and PECAM-1 (green, right panel). Scale bar, 100 µm. (C) Representative images of lung sections at 28 d after elastase instillation in conditions where EC expression of Lrg1 is either intact (Lrg1^loxp+/+) or lost (Lrg1^iΔEC). Scale bars, 4 mm (upper panel), 300 µm (lower panel). (D) Mean cord length quantification 28 d after elastase instillation in conditions where EC expression of Lrg1 is either intact (Lrg1^loxp+/+) or lost (Lrg1^iΔEC). PBS (n = 8 [Lrg1^loxp^+/+], n = 8 [Lrg1^iΔEC]) and elastase (n = 25 [Lrg1^loxp+/+], n = 25 [Lrg1^iΔEC]). Combined data are from at least three independent experiments. **, P < 0.01; ****, P < 0.0001. VE-Cad, VE-cadherin.