Abstract
The effect of IL-10 on macrophage migration was investigated, including the analysis of protein expression, cytokine secretion and activation of the MAPKs and NF-kB pathway. The expression of endogenic IL-10 was down-regulated in macrophage stimulated with oxLDL for indicated time. Exogenous IL-10 reversed oxLDL-inhibited chemotactic macrophage numbers by 48.18±4.93% (3h), 64.8±5.61% (6h) and 63.66±3.05% (12h), and pretreated with SB203580 (P38 signaling inhibitor) in macrophage, oxLDL could not inhibit macrophage emigration. IL-10 significantly decreased oxLDL-mediated increase of SR-A expression, and pretreatment with β-arrestin2 RNAi in macrophage could not change oxLDL-induced SR-A expression. IL-10 also significantly decreased oxLDL-mediated increase of β-arrestin2 expression, and pre-treated with SR-A RNAi in macrophage, oxLDL could not induce the increase of β-arrestin2 expression. However, IL-10 significantly reversed oxLDL-mediated inhibition of CCR7 expression about 95.78±0.99% (mRNA) and 80.06±19.46% (protein), and pretreated with P38 inhibitor SB203580 in macrophage, oxLDL could not decrease CCR7 expression. IL-10 inhibited oxLDL-mediated inhibition of MMP9 secretion about 74.02±22.35%, and pretreated with P38 inhibitor SB203580 in macrophage, oxLDL could not decrease MMP9 secretion. Treatment with oxLDL increased P38-phosphorylation by 31.88±2.79%, 40.24±5.69% and 30.93±4.66% at 15, 30 and 60min, respectively, whereas the effect of IL-10 on the expression of phosphorylated P38 was reversed by 49.49±12.12%, 70.93±16.14% and 47.62±6.00% in up-indicated time-points, respectively. From these data, we speculated oxLDL-SR-A-β-arrestin2-P38-MMP9/CCR7 could play a critical role in the macrophages migration, which was blocked by IL-10 through inhibiting oxLDL uptake.
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