Figure 8.

Dedicator of cytokinesis 2 (DOCK2) attenuates tumor necrosis factor-α (TNF-α)–induced lung fibroblast proinflammatory phenotypic changes through phosphatidylinositol 3-kinase/AKT and NF-κB pathways. A and B: Primary human lung fibroblasts (HLFs) were pretreated with LY294002 (1 μg/mL) (A) or pyrrolidine dithiocarbamate (PDTC) (1 μg/mL) (B) for 30 minutes, followed by TNF-α treatment to detect monocyte chemoattractant protein-1 (MCP-1) and α-tubulin expression. C and D: Quantification of protein expression shown in A (C) and B (D). E: Primary HLFs were infected with adenovirus scramble (Ad-shCtrl) or DOCK2 shRNA (Ad-shDOCK2) and treated with TNF-α for various times to detect phosphor (p-) and total AKT and NF-κB. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) was used as a loading control. n = 3. ∗P < 0.05 versus vehicle-treated group; †P < 0.05 versus TNF-α–treated group.