Fig. 7
From: Chemokine CXCL12 drives pericyte accumulation and airway remodeling in allergic airway disease
LIT-927 abrogates pericyte migration and mitigates airway smooth muscle thickening. Female C57/Bl6 mice (6–8 weeks old) were subjected to intranasal delivery of sterile PBS (10 µl) or house dust mite extract (HDM; 25 µg in 10 µl) 5 days a week for 5 consecutive weeks. A At the end of the protocol, lung sections obtained from PBS control and HDM-exposed mice were stained for α-smooth muscle actin (α-SMA; red) to assess the impact of LIT treatment on airway smooth muscle remodeling. Inset, negative control; scale bar 50 µm. B Airway smooth muscle thickness was quantified morphometrically using ImageJ software. n = 6–9 per group from two independent experiments; ***p < 0.001. Human placental pericytes were subjected to C. Transwell migration assays were used to assess cell migration to CXCL12 (300 ng/ml) in the absence or presence of the CXCL12 neutraligand LIT-927 and the p38 MAPK inhibitor SB203580. n = 5 per group, representative of three independent experiments; **p < 0.01. AW: airway; HDM: house dust mite; LIT: LIT-927 (CXCL12 neutraligand); PBS: phosphate-buffered saline; VEH: vehicle control