RNA-seq analysis provide new insights into mapk signaling of apolipoproteinciii-induced inflammation in porcine vascular endothelial cells

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 in...

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Veröffentlicht in:Cell cycle (Georgetown, Tex.) Tex.), 2017-01, Vol.16 (22), p.2230-2238
Hauptverfasser: Yue, Yuan, Jiang, Hao, Yan, Shouqing, Fu, Yao, Liu, Chang, Sun, Xulei, Chai, Menglong, Gao, Yan, Yuan, Bao, Chen, Chengzhen, Dai, Lisheng, Zhang, Jiabao, Ding, Yu
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container_issue 22
container_start_page 2230
container_title Cell cycle (Georgetown, Tex.)
container_volume 16
creator Yue, Yuan
Jiang, Hao
Yan, Shouqing
Fu, Yao
Liu, Chang
Sun, Xulei
Chai, Menglong
Gao, Yan
Yuan, Bao
Chen, Chengzhen
Dai, Lisheng
Zhang, Jiabao
Ding, Yu
description 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.
doi_str_mv 10.1080/15384101.2017.1373222
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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. 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subjects Animals
Apolipoprotein C-III - pharmacology
Endothelial Cells - metabolism
Inflammation
Interleukin-6 - metabolism
Mitogen-Activated Protein Kinase 1 - genetics
Mitogen-Activated Protein Kinase 1 - metabolism
Mitogen-Activated Protein Kinase 3 - genetics
Mitogen-Activated Protein Kinase 3 - metabolism
Phosphorylation
Signal Transduction - physiology
Swine
Tumor Necrosis Factor-alpha - metabolism
Vascular Cell Adhesion Molecule-1 - genetics
Vascular Cell Adhesion Molecule-1 - metabolism
title RNA-seq analysis provide new insights into mapk signaling of apolipoproteinciii-induced inflammation in porcine vascular endothelial cells
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