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Fig. 2 | Inflammation and Regeneration

Fig. 2

From: CXCL10 deficiency limits macrophage infiltration, preserves lung matrix, and enables lung growth in bronchopulmonary dysplasia

Fig. 2

Loss of CXCL10 enables lung growth and preserves survival of alveolar epithelial type 2 cells (AT2) in neonatal mice after hyperoxia. A Experimental setup for assessment of lung morphometry and lung cell survival in newborn mice exposed to normoxia (21% O2, NOX) or hyperoxia (85% O2, HYX) from birth until postnatal day 14 (P14). B Representative images of hematoxylin and eosin (H&E) stained lung tissue sections of wildtype (WT) and Cxcl10 knockout mice (Cxcl10−/−) at P14. C, D Quantitative histomorphometric analyses for the average surface area of a single alveolus (C) and radial alveolar count (RAC; D). E Representative co-immunofluorescent staining for surfactant protein C (SFTPC; a marker of AT2, red) and TUNEL as an indicator of apoptosis (green) in lungs at P14; DAPI was used for nuclear staining. Quantification of the percentage of TUNEL+ cells (F) and SFTPC + cells relative to all DAPI+ cells (G). Mean ± SEM; n = 3–6/group; Unpaired t test: $p < 0.05; Two-way ANOVA: *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001; scale bars: 20X, 40X

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