Angiotensin II significantly increased endothelial lipase protein expression in human umbilical vein endothelial cells, an effect that was partially inhibited by NF-kB and MAPK p38 inhibitors.
Does Angiotensin II upregulate endothelial lipase expression via NF-κB and MAPK signaling pathways in human umbilical vein endothelial cells?
Angiotensin II upregulates endothelial lipase expression in human umbilical vein endothelial cells via the NF-κB and MAPK signaling pathways, providing a potential molecular link between the renin-angiotensin system and atherosclerosis.
p-value: p=<0.05
BACKGROUND: 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). METHODS AND FINDINGS: 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. CONCLUSION: AngII may upregulate EL protein expression via the NF-κB and MAPK signaling pathways.
Zhang et al. (2014) studied Atherosclerosis mechanism (in vitro). Angiotensin II vs. Control group without any treatment was evaluated on Endothelial lipase (EL) protein expression levels (p=<0.05). Angiotensin II significantly increased endothelial lipase protein expression in human umbilical vein endothelial cells, an effect that was partially inhibited by NF-kB and MAPK p38 inhibitors.
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