Advanced Glycation End Products Enhance Murine Monocyte Proliferation in Bone Marrow and Prime Them into an Inflammatory Phenotype through MAPK Signaling

Figure 5

Block of the p38 or ERK pathway attenuated AGE-induced monocyte proliferation and proinflammatory activation. Cells were divided into four groups (control, AGEs, AGEs + SB203580, and AGEs + U0126). The control group was treated with BSA and the AGE group with AGEs (300 μg/mL), while the next two groups were pretreated with SB203580 (specific inhibitor of p38) or U0126 (specific inhibitor of ERK) for 60 min and then treated with AGEs (300 μg/mL) during a 24 h incubation. For (a) and (b), the 4 groups of cells were harvested and RNA was extracted for real-time PCR tests. (a) Block of p38 or ERK pretreatment attenuated AGE-induced proinflammatory cytokine (IL-1β and TNF-α) expression. (b) Block of p38 or ERK pretreatment attenuated AGE-induced mRNA expression of GM-CSF. For (c), cells were prepared for IF staining for Ki67. (c) Block of p38 or ERK pretreatment abated AGE-induced Ki67 expression in monocytes. Bar graphs represent the results (mean ± SD) of four independent experiments. , , and , in between-group comparisons.

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