A calpain inhibitor protects against fractalkine production in lipopolysaccharide-treated endothelial cells
Kidney Research and Clinical Practice
;
: 224-231, 2017.
Artigo
em Inglês
| WPRIM
| ID: wpr-218955
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.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Calpaína
/
Sobrevivência Celular
/
Lipopolissacarídeos
/
Interleucinas
/
Fator de Necrose Tumoral alfa
/
Apoptose
/
Endotoxemia
/
Células Endoteliais
/
Caspase 3
/
Caspase 9
Idioma:
Inglês
Revista:
Kidney Research and Clinical Practice
Ano de publicação:
2017
Tipo de documento:
Artigo
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