[The role of p38 MAPK in LPS induced ICAM-1 expression on endothelial cell].
Wensheng Yan, Yinong Jiang, Qun Huang
Abstract
Wensheng Yan, Yinong Jiang, Qun Huang
Abstract
OBJECTIVE: To study the role of p38 mitogen-activated protein kinase (MAPK) in lipopolysaccharide (LPS) induced expression of intercellular adhesion molecule-1 (ICAM-1) on human umbilical vein endothelial cell (HUVEC). METHODS: HUVEC was harvested and cultured before being divided into two groups, i,e. stimulating group (S) and priming group (P). In S group, the cultured endothelial cell was stimulated by LPS. In P group, endothelial cell was pre-treated with SB 203580 2 hours before LPS stimulation. The expressions of ICAM-1 mRNA and protein in HUVEC of two groups and their dose-effect relationship with stimulator and inhibitor were observed. Furthermore the p38 mRNA activity of HUVEC was detected. RESULTS: After LPS stimulation, ICAM-1 molecule on the surface of endothelium increased significantly at 8 to 36 hours. Cytoplasmic mRNA increased obviously at 2 hours. The activity of p38 MAPK increased at 15 min and reached peak value at 30 to 60 min after that HUVEC was stimulated by LPS. CONCLUSION: Inhibitor SB 203580 of p38 might significantly inhibit the inducing effect of LPS. LPS could regulate the expression of ICAM-1 gene and protein in HUVEC by activating p38 MAPK signal transduction passage.
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OBJECTIVE: To study the role of p38 mitogen-activated protein kinase (MAPK) in lipopolysaccharide (LPS) induced expression of intercellular adhesion molecule-1 (ICAM-1) on human umbilical vein endothelial cell (HUVEC). METHODS: HUVEC was harvested and cultured before being divided into two groups, i,e. stimulating group (S) and priming group (P). In S group, the cultured endothelial cell was stimulated by LPS. In P group, endothelial cell was pre-treated with SB 203580 2 hours before LPS stimulation. The expressions of ICAM-1 mRNA and protein in HUVEC of two groups and their dose-effect relationship with stimulator and inhibitor were observed. Furthermore the p38 mRNA activity of HUVEC was detected. RESULTS: After LPS stimulation, ICAM-1 molecule on the surface of endothelium increased significantly at 8 to 36 hours. Cytoplasmic mRNA increased obviously at 2 hours. The activity of p38 MAPK increased at 15 min and reached peak value at 30 to 60 min after that HUVEC was stimulated by LPS. CONCLUSION: Inhibitor SB 203580 of p38 might significantly inhibit the inducing effect of LPS. LPS could regulate the expression of ICAM-1 gene and protein in HUVEC by activating p38 MAPK signal transduction passage.
Key concepts: Umbilical vein, p38 mitogen-activated protein kinases, Lipopolysaccharide, ICAM-1, MAPK/ERK pathway, Endothelial stem cell, Molecular biology, Endothelium