title: Gene expression of adhesion molecules in pulmonary and hepatic microvascular endothelial cells during sepsis.
abstract: OBJECTIVE
  To study the gene expression of adhesion molecules in pulmonary and hepatic microvascular endothelial cells during sepsis in mice.
  
  
  METHODS
  Male mice were subjected to cecal ligation and puncture (CLP) and microvascular endothelial cells in pulmonary and hepatic tissues were harvested at 3 hours (early sepsis) and 12 hours (late sepsis) after CLP, respectively. Gene expression of the adhesion molecules was assessed by reverse transcription  polymerase chain reaction (RT-PCR). Simultaneously, the alterations of myeloperoxidase (MPO) activity in pulmonary and hepatic tissues were also examined.
  
  
  RESULTS
  E-selectin mRNA levels markedly increased at 3 hours after CLP in both pulmonary and hepatic microvascular endothelial cells, then they returned to the normal level at 12 hours after CLP. Increases in intercellular adhesion molecule-1 (ICAM-1) mRNA levels were found at 3 hours after CLP in both pulmonary and hepatic microvascular endothelial cells, and these levels became higher at 12 hours after CLP. Adhesion molecule-1 (VCAM-1) mRNA expression of vascular cells also increased significantly at 3 hours and 12 hours after CLP in both pulmonary and hepatic microvascular endothelial cells. The level of VCAM-1 mRNA in hepatic microvascular endothelial cells was higher at 3 hours than that at 12 hours after CLP, while the level of VCAM-1 mRNA in pulmonary microvascular endothelial cells was higher at 12 hours than that at 3 hours after CLP. The MPO activity in pulmonary and hepatic tissues increased at 3 hours after CLP, compared with that of the sham group. They both declined significantly at 12 hours after CLP, but they were still higher than that of the sham group.
  
  
  CONCLUSIONS
  The up-regulation of the gene expression of adhesion molecules in pulmonary and hepatic microvascular endothelial cells is an important step for the migration and accumulation of leukocytes at the site of inflammation, which plays a critical role in organ damage during sepsis. And the contribution of the heterogeneity of endothelial cells in organs' vulnerability during sepsis is worth a further investigation.
authors.affiliation: Institute of Surgical Research, General Hospital of PLA, Beijing 100853, China. wurq@yahoo.com
authors.forename: Rongqian
authors.initials: R
authors.lastname: Wu
authors.forename: Yingxin
authors.initials: Y
authors.lastname: Xu
authors.forename: Xuhua
authors.initials: X
authors.lastname: Song
authors.forename: Xianjun
authors.initials: X
authors.lastname: Meng
mesh_terms: D000818:Animals; D004730:Endothelium, Vascular / Q000166:cytology*; D015870:Gene Expression; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics*; D008099:Liver / Q000166:cytology*; D008168:Lung / Q000166:cytology*; D008297:Male; D051379:Mice; D009195:Peroxidase / Q000378:metabolism; D018805:Sepsis / Q000378:metabolism*; D015854:Up-Regulation; D019010:Vascular Cell Adhesion Molecule-1 / Q000235:genetics*
chemical_list: D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D009195:Peroxidase