Fig. 9: PDGF-BB acts through the PI3K-NF-κB pathway to modify pericyte inflammatory secretions.

Pericytes were treated with vehicle or IL-1β (10 ng/mL), with or without PDGF-BB (10 ng/mL) for 2 h, then fixed and immunostained or 48 h and conditioned media collected for cytometric bead array. a Representative images and quantification of MCP-1 and IL-6 in cells treated with IL-1β or PDGF-BB. n = 3, two-way ANOVA. Scale bar = 100 μm, insert = 10 μm. b Secretion of MCP-1, IL-8, IL-6 and CX3CL1 in cells treated with IL-1β with or without PDGF-BB. Pericytes were pre-treated with PDGFRβ inhibitor sunitinib (100 nM), PI3K inhibitor wortmannin (100 nM) or MEK/ERK inhibitor U0126 (10 μM) or vehicle (0.3% DMSO) for 30 min, then treated with vehicle or PDGF-BB (10 ng/mL) for 48 h, and conditioned media collected. c Quantification of MCP-1, IL-8, IL-6 and CX3CL1 concentrations in conditioned media from pericytes treated with PDGF-BB with or without pathway inhibitors. Pericytes were treated with control siRNA (siNT) or siRNA directed against p65 NF-κB (siRELA) for 96 h, then treated with PDGF-BB (10 ng/mL) for 48 h and conditioned media collected for cytometric bead array. n = 5, two-way ANOVA. d Quantification of MCP-1, IL-8, IL-6 and CX3CL1 concentrations in conditioned media from pericytes treated with PDGF-BB with siRNA against NF-κB. n = 4, two-way ANOVA. *p < 0.05, **p < 0.01, ***p < 0.001 vs vehicle control, #p < 0.05, ##p < 0.01, ###p < 0.001 vs PDGF-BB-treated.