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Fig. 6 | Particle and Fibre Toxicology

Fig. 6

From: Epithelial MAPK signaling directs endothelial NRF2 signaling and IL-8 secretion in a tri-culture model of the alveolar-microvascular interface following diesel exhaust particulate (DEP) exposure

Fig. 6

Alveolar epithelial MAPK signaling activates microvascular endothelial NRF2-dependent antioxidant gene expression. A Illustrated representation of epithelial cell MAPK inhibition pre-treatment with the ERK1/2 inhibitor, SCH772984, and the p38 inhibitor, LY2228820 (ERKi/p38i). B Protein expression and densitometry of phosphorylated and total ERK1/2, p38, MK2, and vinculin (loading control), in epithelial cells after a 1 h ACRE-DEP exposure. Note: the outlined p-MK2 and t-MK2 blots are from the same immunoblot as the shown VEH and DEP bands; however, they were not originally ordered in the same pattern as the other samples in B, thus the bands outlined with the black border were re-ordered as shown. C Protein expression and densitometry of NRF2 stabilization and GAPDH (loading control) in endothelial cells after a 2 h ACRE-DEP exposure. D mRNA expression of HMOX1, NQO1, and GCLM in endothelial cells after a 6 h ACRE-DEP exposure. B–D Values represent the mean of n = 3 independent experiments ± SD and immunoblots are representative images from n = 3 independent experiments. Statistically significant differences between VEH, ACRE-DEP, and DEP + ERKi/p38i cells are indicated by *p ≤ .05 and ****p ≤ .0001

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