Study on visfatin-induced inflammation and necroptosis via LOX-1 in human umbilical vein endothelial cells.
10.7507/1001-5515.202003067
- Author:
Xiaoyu HAN
1
,
2
;
Wenchao WU
2
;
Xiaojing LIU
3
,
4
;
Ye ZHU
4
Author Information
1. Geriatrics Department, Chengdu Second People's Hospital, Chengdu 610017, P.R.China
2. Laboratory of Cardiovascular Diseases, West China Hospital, Sichuan University, Chengdu 610041, P.R.China.
3. Laboratory of Cardiovascular Diseases, West China Hospital, Sichuan University, Chengdu 610041, P.R.China
4. Vasculocardiology Department, West China Hospital, Sichuan University, Chengdu 610041, P.R.China.
- Publication Type:Journal Article
- Keywords:
LOX-1;
human umbilical vein endothelial cells;
inflammation;
necroptosis;
visfatin
- MeSH:
Cells, Cultured;
Human Umbilical Vein Endothelial Cells;
Humans;
Inflammation/chemically induced*;
Necroptosis;
Nicotinamide Phosphoribosyltransferase;
Scavenger Receptors, Class E/genetics*
- From:
Journal of Biomedical Engineering
2020;37(5):834-841
- CountryChina
- Language:Chinese
-
Abstract:
The aim of the study is to identify the effects and underlying mechanisms of visfatin on inflammation and necroptosis in vascular endothelial cells. Human umbilical vein endothelial cells (HUVECs) were stimulated with visfatin or pretreated with Polyinosinic acid (LOX-1 inhibitor). By using the Western blot, RT-PCR, immunocytochemistry, enzyme-linked immunosorbent assay (ELISA), MTT and flow cytometry technique, the occurrence of inflammation and necroptosis in HUVECs were evaluated. Our results showed that 100 ng/mL visfatin significantly increased the mRNA and protein expression of monocyte chemotactic protein 1 (MCP-1) and LOX-1 after 24 hours' treatment in HUVECs. However, pretreatment with Polyinosinic acid could significantly reduce the expression of MCP-1 compared with visfatin group. Additionally, 100 ng/mL visfatin could induce the production of necrotic features and increase the mRNA expression of BMF (one of the markers of necroptosis), while pretreating with Polyinosinic acid markedly downregulated the mRNA expression of BMF gene and promoted the cell proliferation. These results indicate that visfatin might induce inflammation and necroptosis via LOX-1 in HUVECs, suggesting that visfatin plays a central role in the development of atherosclerosis.
