Figure 4
Figure 4. p16INK4a deficiency modulates macrophage responses to alternatively and classically polarizing stimuli. mRNA expression from p16+/+ and p16−/− BMDM activated with 15 ng/mL IL-4 during 24 hours (A-C), 10 ng/mL IFNγ during 12 hours (D-F), or 100 ng/mL LPS during 2 hours (G) or 24 hours (H-I). mRNA expression of the IL-4–induced target genes Arg-I (A), Ym1/2 (B), and Mgl2 (C); IFNγ-induced target genes iNOS (D), Cxcl10 (E), and MHCII (F); and LPS-induced target genes TNF (G), IL-6 (H), and MCP-1 (I) was quantified by QPCR and expressed as fold increase compared with respective controls. Statistically significant differences are indicated (t test; ***P < .001 **P < .01, and *P < .05).

p16INK4a deficiency modulates macrophage responses to alternatively and classically polarizing stimuli. mRNA expression from p16+/+ and p16−/− BMDM activated with 15 ng/mL IL-4 during 24 hours (A-C), 10 ng/mL IFNγ during 12 hours (D-F), or 100 ng/mL LPS during 2 hours (G) or 24 hours (H-I). mRNA expression of the IL-4–induced target genes Arg-I (A), Ym1/2 (B), and Mgl2 (C); IFNγ-induced target genes iNOS (D), Cxcl10 (E), and MHCII (F); and LPS-induced target genes TNF (G), IL-6 (H), and MCP-1 (I) was quantified by QPCR and expressed as fold increase compared with respective controls. Statistically significant differences are indicated (t test; ***P < .001 **P < .01, and *P < .05).

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