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Fig. 1 | Inflammation and Regeneration

Fig. 1

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

Fig. 1

CXCL10 is a central hub of the inflammatory network of hyperoxia-induced lung injury in newborn mice. A Experimental setup for transcriptomic analysis of lungs of newborn mice exposed to normoxia (21% O2, NOX) or hyperoxia (80% O2, HYX) from birth until postnatal day 14 (P14). B, C: Heatmap (B) and pathways analysis (C). The heatmap contains the top 25 up- and downregulated differentially expressed genes (DEG; p < 0.05 and log fold change > 1.5), n = 6 per group. D Sneaky plot for DEGs association with (GO) Biological Process. E Assessment of gene expression of Cxcl10 (C-X-C motif chemokine 10) using quantitative RT-PCR in lungs of newborn mice exposed to NOX (black bars) or HYX (white bars) from birth until P7 or P28; n = 11–12 per group. F Quantification of CXCL10 protein concentration using ELISA in serum of mice exposed to NOX or HYX from birth until P14. G Measurement of mRNA expression of Cxcr3 (C-X-C Motif Chemokine Receptor 3) in lungs exposed to NOX or HYX from birth until P7 or 28. Mean ± SEM; n = 3–6/group; Mann–Whitney test: #p < 0.05; ####p < 0.0001, Unpaired t test $p < 0.05

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