Endothelial lipase is upregulated by interleukin-6 partly via the p38 MAPK and p65 NF-κB signaling pathways.

Abstract

To investigate the effects of inflammatory factor interleukin (IL)‑6 on the expression of endothelial lipase (EL) and its potential signaling pathways in atherosclerosis, a primary culture of human umbilical vein endothelial cells (HUVECs) was established and treated as follows: i) Control group without any treatment; ii) recombinant human (rh)IL‑6 treatment (10 ng/ml) for 0, 4, 8, 12 and 24 h; iii) p38 mitogen‑activated protein kinases (MAPKs) inhibitor (SB203580, 10 µmol/l) pretreatment for 1 h prior to rhIL‑6 (10 ng/ml) treatment; iv) nuclear factor (NF)‑κB activation inhibitor (pyrrolidine dithiocarbamate, 10 mmol/l) pretreatment for 1 h prior to rhIL‑6 (10 ng/ml) treatment. EL levels were detected by immunocytochemical staining and western blot analysis. Proliferation of HUVECs was detected by immunostaining of proliferating cell nuclear antigen (PCNA) and an MTT assay. p38 MAPK and NF‑κB p65 levels were detected by western blotting. The results showed that rhIL‑6 treatment increased EL expression and proliferation of HUVECs. NF‑κB p65 and MAPK p38 protein levels also increased in a time‑dependent manner in HUVECs after rhIL‑6 treatment. NF‑κB inhibitor and MAPK p38 inhibitor prevented the effects of rhIL‑6 on EL expression. In conclusion, inflammatory factor IL‑6 may participate in the pathogenesis of atherosclerosis by increasing EL expression and the proliferation of endothelial cells via the p38 MAPK and NF-κB signaling pathways.

• Authors: Xin Yue, Minghui Wu, Hong Jiang, Jing Hao, Qinghao Zhao, Qing Zhu, Gaowa Saren, Yun Zhang, Xiaoli Zhang
• Journal: Molecular medicine reports (Mol Med Rep) Vol. 14 Issue 3 Pg. 1979-85 (Sep 2016) ISSN: 1791-3004 [Electronic] Greece
• PMID: 27430252 (Publication Type: Journal Article)

Chemical References

• IL6 protein, human
• Interleukin-6
• NF-kappa B
• p38 Mitogen-Activated Protein Kinases
• LIPG protein, human
• Lipase

Topics

• Atherosclerosis (etiology)
• Cell Proliferation
• Human Umbilical Vein Endothelial Cells (metabolism, physiology)
• Humans
• Infant, Newborn
• Interleukin-6
• Lipase (genetics)
• NF-kappa B
• Signal Transduction
• Up-Regulation
• p38 Mitogen-Activated Protein Kinases