Effect of sphingosine 1-phosphate/sphingosine 1-phosphate receptor signal pathway on function of neutrophils.
- Author:
Zhong-Ying WANG
1
;
Ru-Feng XIE
;
Jie YANG
;
Ya-Na REN
;
Yi-Ming YANG
;
Hua-Hua FAN
Author Information
1. Department of Biology and Medicine, East China Normal University, Shanghai, China.
- Publication Type:Journal Article
- MeSH:
Cells, Cultured;
Humans;
Lysophospholipids;
metabolism;
NADPH Oxidases;
metabolism;
Neutrophils;
metabolism;
physiology;
Proto-Oncogene Proteins c-akt;
metabolism;
Receptors, Lysosphingolipid;
metabolism;
Respiratory Burst;
Signal Transduction;
Sphingosine;
analogs & derivatives;
metabolism;
Superoxides;
metabolism
- From:
Journal of Experimental Hematology
2012;20(4):989-994
- CountryChina
- Language:Chinese
-
Abstract:
The aim of this study was to examine the priming effect of sphingosine 1-phosphate (S1P) on fMLP-activated neutrophils, mainly to detect the neutrophil respiratory burst products, and to investigate the signaling pathway involved in S1P activity. Flow cytometry was used to evaluate the new isolated neutrophil; the superoxide anion output was detected indirectly by cytochrome C reduction in respiratory burst; the dihydro-rhodamine 123 was used to detect the intensity of respiratory burst; the signal transduction pathways of neutrophil respiratory burst were explored by Western blot. The results showed that after pretreated with S1P, the level of superoxide anion released by fMLP-activated neutrophils significantly increased; the Rhodamine 123 mean fluorescence intensity in S1P primed fMLP-activated neutrophils group was significantly higher than that in fMLP treatment group; PI3K and Akt proteins involved in the signal pathway of neutrophil respiratory burst. It is concluded that S1P is a new priming reagent, which primes respiratory burst of fMLP-activated neutrophils; this signal pathway may be that S1P interacts with its receptor, activates PI3K, then activates Akt-transmitting signals through NADPH oxidase, finally results in the respiratory burst.