A calpain inhibitor protects against fractalkine production in lipopolysaccharide-treated endothelial cells.
10.23876/j.krcp.2017.36.3.224
- Author:
Jaewoong JANG
1
;
Yoosik YOON
;
Dong Jin OH
Author Information
1. Department of Microbiology, Chung-Ang University College of Medicine, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Calpain;
Caspase;
CX3CL1;
Endothelial cells;
Lipopolysaccharides
- MeSH:
Apoptosis;
Calpain*;
Caspase 3;
Caspase 9;
Cell Survival;
Chemokine CX3CL1*;
Endothelial Cells*;
Endotoxemia;
Human Umbilical Vein Endothelial Cells;
Interleukins;
Lipopolysaccharides;
Tumor Necrosis Factor-alpha
- From:Kidney Research and Clinical Practice
2017;36(3):224-231
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: Fractalkine (CX3CL1) is a chemokine with a unique CX3C motif and is produced by endothelial cells stimulated with lipopolysaccharide (LPS), tumor necrosis factor (TNF)-α, interleukin (IL)-1, and interferon-γ. There have been several reports that the caspase/calpain system is activated in endotoxemia, which leads to cellular apoptosis and acute inflammatory processes. We aimed to determine the role of the caspase/calpain system in cell viability and regulation of fractalkine production in LPS-treated endothelial cells. METHODS: Human umbilical vein endothelial cells (HUVECs) were stimulated with 0.01–100 μg/mL of LPS to determine cell viability. The changes of CX3CL1 expression were compared in control, LPS (1 μg/mL)-, IL-1α (1 μg/mL)-, and IL-1β (1 μg/mL)-treated HUVECs. Cell viability and CX3CL1 production were compared with 50 μM of inhibitors of caspase-1, caspase-3, caspase-9, and calpain in LPS-treated HUVECs. RESULTS: Cell viability was significantly decreased from 1 to 100 μg/mL of LPS. Cell viability was significantly restored with inhibitors of caspase-1, caspase-3, caspase-9, and calpain in LPS-treated HUVECs. The expression of CX3CL1 was highest in IL-1β-treated HUVECs. CX3CL1 production was highly inhibited with a calpain inhibitor and significantly decreased with the individual inhibitors of caspase-1, caspase-3, and caspase-9. CONCLUSION: The caspase/calpain system is an important modulator of cell viability and CX3CL1 production in LPS-treated endothelial cells.
