Angiotensin II upregulates endothelial lipase expression via the NF-kappa B and MAPK signaling pathways.

<h4>Background</h4>Angiotensin II (AngII) participates in endothelial damage and inflammation, and accelerates atherosclerosis. Endothelial lipase (EL) is involved in the metabolism and clearance of high density lipoproteins (HDL), the serum levels of which correlate negatively with the...

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Autores principales: Xiaoli Zhang, Minghui Wu, Hong Jiang, Jing Hao, Qingli Zhang, Qing Zhu, Gaowa Saren, Yun Zhang, Xiaohui Meng, Xin Yue
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Publicado: Public Library of Science (PLoS) 2014
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spelling oai:doaj.org-article:4f8fc572e51442bb99b15b790714a6162021-11-25T05:59:32ZAngiotensin II upregulates endothelial lipase expression via the NF-kappa B and MAPK signaling pathways.1932-620310.1371/journal.pone.0107634https://doaj.org/article/4f8fc572e51442bb99b15b790714a6162014-01-01T00:00:00Zhttps://doi.org/10.1371/journal.pone.0107634https://doaj.org/toc/1932-6203<h4>Background</h4>Angiotensin II (AngII) participates in endothelial damage and inflammation, and accelerates atherosclerosis. Endothelial lipase (EL) is involved in the metabolism and clearance of high density lipoproteins (HDL), the serum levels of which correlate negatively with the onset of cardiovascular diseases including atherosclerosis. However, the relationship between AngII and EL is not yet fully understood. In this study, we investigated the effects of AngII on the expression of EL and the signaling pathways that mediate its effects in human umbilical vein endothelial cells (HUVECs).<h4>Methods and findings</h4>HUVECs were cultured in vitro with different treatments as follows: 1) The control group without any treatment; 2) AngII treatment for 0 h, 4 h, 8 h, 12 h and 24 h; 3) NF-κB activation inhibitor pyrrolidine dithiocarbamate (PDTC) pretreatment for 1 h before AngII treatment; and 4) mitogen-activated protein kinase (MAPK) p38 inhibitor (SB203580) pretreatment for 1 h before AngII treatment. EL levels in each group were detected by immunocytochemical staining and western blotting. HUVECs proliferation was detected by MTT and proliferating cell nuclear antigen (PCNA) immunofluorescence staining. NF-kappa B (NF-κB) p65, MAPK p38, c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK) and phosphorylated extracellular signal-regulated kinase (p-ERK) expression levels were assayed by western blotting. The results showed that the protein levels of EL, NF-κB p65, MAPK p38, JNK, and p-ERK protein levels, in addition to the proliferation of HUVECs, were increased by AngII. Both the NF-kB inhibitor (PDTC) and the MAPK p38 inhibitor (SB203580) partially inhibited the effects of AngII on EL expression.<h4>Conclusion</h4>AngII may upregulate EL protein expression via the NF-κB and MAPK signaling pathways.Xiaoli ZhangMinghui WuHong JiangJing HaoQingli ZhangQing ZhuGaowa SarenYun ZhangXiaohui MengXin YuePublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 9, p e107634 (2014)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Xiaoli Zhang
Minghui Wu
Hong Jiang
Jing Hao
Qingli Zhang
Qing Zhu
Gaowa Saren
Yun Zhang
Xiaohui Meng
Xin Yue
Angiotensin II upregulates endothelial lipase expression via the NF-kappa B and MAPK signaling pathways.
description <h4>Background</h4>Angiotensin II (AngII) participates in endothelial damage and inflammation, and accelerates atherosclerosis. Endothelial lipase (EL) is involved in the metabolism and clearance of high density lipoproteins (HDL), the serum levels of which correlate negatively with the onset of cardiovascular diseases including atherosclerosis. However, the relationship between AngII and EL is not yet fully understood. In this study, we investigated the effects of AngII on the expression of EL and the signaling pathways that mediate its effects in human umbilical vein endothelial cells (HUVECs).<h4>Methods and findings</h4>HUVECs were cultured in vitro with different treatments as follows: 1) The control group without any treatment; 2) AngII treatment for 0 h, 4 h, 8 h, 12 h and 24 h; 3) NF-κB activation inhibitor pyrrolidine dithiocarbamate (PDTC) pretreatment for 1 h before AngII treatment; and 4) mitogen-activated protein kinase (MAPK) p38 inhibitor (SB203580) pretreatment for 1 h before AngII treatment. EL levels in each group were detected by immunocytochemical staining and western blotting. HUVECs proliferation was detected by MTT and proliferating cell nuclear antigen (PCNA) immunofluorescence staining. NF-kappa B (NF-κB) p65, MAPK p38, c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK) and phosphorylated extracellular signal-regulated kinase (p-ERK) expression levels were assayed by western blotting. The results showed that the protein levels of EL, NF-κB p65, MAPK p38, JNK, and p-ERK protein levels, in addition to the proliferation of HUVECs, were increased by AngII. Both the NF-kB inhibitor (PDTC) and the MAPK p38 inhibitor (SB203580) partially inhibited the effects of AngII on EL expression.<h4>Conclusion</h4>AngII may upregulate EL protein expression via the NF-κB and MAPK signaling pathways.
format article
author Xiaoli Zhang
Minghui Wu
Hong Jiang
Jing Hao
Qingli Zhang
Qing Zhu
Gaowa Saren
Yun Zhang
Xiaohui Meng
Xin Yue
author_facet Xiaoli Zhang
Minghui Wu
Hong Jiang
Jing Hao
Qingli Zhang
Qing Zhu
Gaowa Saren
Yun Zhang
Xiaohui Meng
Xin Yue
author_sort Xiaoli Zhang
title Angiotensin II upregulates endothelial lipase expression via the NF-kappa B and MAPK signaling pathways.
title_short Angiotensin II upregulates endothelial lipase expression via the NF-kappa B and MAPK signaling pathways.
title_full Angiotensin II upregulates endothelial lipase expression via the NF-kappa B and MAPK signaling pathways.
title_fullStr Angiotensin II upregulates endothelial lipase expression via the NF-kappa B and MAPK signaling pathways.
title_full_unstemmed Angiotensin II upregulates endothelial lipase expression via the NF-kappa B and MAPK signaling pathways.
title_sort angiotensin ii upregulates endothelial lipase expression via the nf-kappa b and mapk signaling pathways.
publisher Public Library of Science (PLoS)
publishDate 2014
url https://doaj.org/article/4f8fc572e51442bb99b15b790714a616
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