[The significance of the expression of endothelial ICAM-1 induced by LPS].
OBJECTIVE
To investigate the significance of the expression pattern and its signal modulating mechanism of endothelial ICAM-1 induced by LPS.


METHODS
(1) The expression pattern of the ICAM-1 was observed at mRNA level in cultured human umbilical vascular endothelial cells (HUVECs) strain ECV-304 after being stimulated by different LPS concentrations at different time points. (2) The modulating effects of different signal pathways on the ICAM-1 expression of the HUVECs were observed at mRNA and protein levels under the stimulation of LPS after the cells were primed by signal pathway blocking agents for 30 mins.


RESULTS
(1) The ICAM-1 mRNA expression could be induced by LPS (100 pg/ml) for 6 hours, and the expression was enhanced along with the increase of LPS concentration. The expression peaked when LPS was at concentrations of 100 approximately 1 000 ng/ml. Temporally, the mRNA expression reached the top level at 6 approximately 8 hours and remained high 12 hours after the stimulation. (2) The expressions of ICAM-1 mRNA and protein could be significantly inhibited by PSI, the NF-kappaB inhibitor. Moreover, the expression of ICAM-1 could all be partially inhibited at mRNA and protein levels by PD98059, the ERK1/2MAPK inhibitor, as well as SB203580, the p38MAPK inhibitor.


CONCLUSIONS
The ICAM-1 mRNA expression of HUVECs could be induced by LPS in both dose and time dependent manner. NF-kappaB might be the major signal pathway of modulating ICAM-1 expression, and p38 and ERK1/2 could possibly be signal pathways of minor importance.
Shan
Youan
Y
Institute of Burn Research, Southwestern Hospital, The Third Military Medical University, Chongqing, 400038, P.R. China.
Su
Yongyue
Y
Luo
Xiangdong
X
Yang
Zongcheng
Z
D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D005786:Gene Expression Regulation / Q000187:drug effects*; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics*; D008070:Lipopolysaccharides / Q000633:toxicity*; D020928:Mitogen-Activated Protein Kinases / Q000502:physiology; D016328:NF-kappa B / Q000502:physiology; D015398:Signal Transduction; D013997:Time Factors
D008070:Lipopolysaccharides; D016328:NF-kappa B; D018799:Intercellular Adhesion Molecule-1; D020928:Mitogen-Activated Protein Kinases