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. Author manuscript; available in PMC: 2017 Jun 19.
Published in final edited form as: Circ Res. 2011 Aug 11;109(7):739–749. doi: 10.1161/CIRCRESAHA.111.245530

Figure 6. Prdx2 deficiency increases MCP-1 production and leukocyte transmigration.

Figure 6

A, TNF-α–induced MCP-1 secretion in isolated aortas from Prdx2−/− mice is increased compared with Prdx2+/+ mice. Isolated aortas were cultured with or without TNF-α (10 ng/mL) for 12 hours and media were analyzed by ELISA (mean±SEM; n=5to7). *P<0.05, **P<0.01 compared with control group. B, TNF-α–induced MCP-1 secretion by isolated aortas of Prdx2−/− mice. Isolated aortas were cultured with or without TNF-α (10 ng/mL) for 12 hours with or without inhibitors. *P<0.05, **P<0.01, ***P<0.001 relative to Prdx2−/− mice treated with TNF-α. C and D, In vitro transmigration assay. MAECs from Prdx2+/+ and Prdx2−/− mice in transwells were activated by TNF-α (10 ng/mL) for 6 hours. Inhibitors were added to MAECs for 1 hour before TNF-α treatment. After 4 hours (C)or18 hours (D), CD11b+ monocytes that transmigrated into the low chamber were counted. *P<0.05 compared with Prdx2+/+ controls. #P<0.05, ##P<0.01, ###P<0.001 compared with Prdx2−/− MAECs without inhibitors. E, Representative confocal images for analyzing in vitro transmigration rate after 10 minutes and quantitative graph. Arrow indicates the CD11b+ monocyte. Transmigration rate was estimated as percentage of transmigration depth of leukocyte over endothelial layer thickness and was accelerated in Prdx2-deficient MAECs after 10 minutes.*P<0.05 compared with counterpart.