a College of Animal Sciences, Jilin University , Changchun , Jilin , China.
b Embryo Centre, Shenyang Jiuzhou Hosipital , Shenyang , Liaoning , China.
Cell Cycle. 2017;16(22):2230-2238. doi: 10.1080/15384101.2017.1373222. Epub 2017 Sep 21.
Apolipoprotein CIII (ApoCIII) has been shown to be associated with the inflammatory response, but the mechanism of its inflammatory effects remains unclear. Because vascular endothelial cells (VECs) play a key role in the development of inflammation, the present study was performed to investigate inflammatory mechanisms induced by ApoCIII in VECs. In this study, we screened differentially expressed genes (DEGs) using RNA-sequencing. The results identified 390 up-regulated genes and 257 down-regulated genes. We performed GO functional classification and KEGG pathway analysis for DEGs. Analysis of sequencing data showed that 21 genes were related to the MAPK pathway. Finally, we investigated whether ApoCIII regulates the expression of pro-inflammatory cytokines via MAPK signaling pathway. The results showed that ApoCIII increased the expression levels of IL-6, TNF-α, VCAM-1 and ICAM-1 in VECs. ApoCIII activated the phosphorylation of ERK1/2 and p38 MAPK. An inhibitor of ERK1/2 and p38 MAPK decreased the protein levels of IL-6 and TNF-α. Our findings demonstrate that ApoCIII induces pro-inflammatory cytokine production in VECs via activation of ERK1/2 and p38 MAPK phosphorylation.
载脂蛋白 CIII（ApoCIII）已被证明与炎症反应有关，但它的炎症作用机制尚不清楚。由于血管内皮细胞（VECs）在炎症的发展中起着关键作用，因此本研究旨在研究 ApoCIII 在 VECs 中引起的炎症机制。在这项研究中，我们使用 RNA 测序筛选差异表达基因（DEGs）。结果确定了 390 个上调基因和 257 个下调基因。我们对 DEGs 进行了 GO 功能分类和 KEGG 途径分析。测序数据分析表明，有 21 个基因与 MAPK 途径有关。最后，我们研究了 ApoCIII 是否通过 MAPK 信号通路调节促炎细胞因子的表达。结果表明，ApoCIII 增加了 VECs 中 IL-6、TNF-α、VCAM-1 和 ICAM-1 的表达水平。ApoCIII 激活了 ERK1/2 和 p38 MAPK 的磷酸化。ERK1/2 和 p38 MAPK 的抑制剂降低了 IL-6 和 TNF-α的蛋白水平。我们的研究结果表明，ApoCIII 通过激活 ERK1/2 和 p38 MAPK 磷酸化诱导 VECs 中促炎细胞因子的产生。
