title: Platelet-endothelial cell adhesion molecule-1 gene expression in liver sinusoidal endothelial cells during liver injury and repair.
abstract: OBJECTIVE
  Platelet-endothelial cell adhesion molecule (PECAM)-1 is suggested to be critical for transmigration processes. It is a matter of debate whether PECAM-1 is expressed in liver sinusoids and whether it is involved in liver inflammation.
  
  
  METHODS
  Indirect immunostaining and in situ hybridization was used to analyze PECAM-1 gene expression in normal and diseased rat and human livers as well as in isolated rat sinusoidal endothelial cells (SECs), hepatic stellate cells and hepatocytes. At various time points after the administration of CCl4 (6 h, 24 h, 48 h, and 72 h), PECAM-1 gene expression was analyzed in livers and in SECs by immunostaining, and Northern blot analysis.
  
  
  RESULTS
  In normal rat or human livers PECAM-1 immunoreactivity was detected along the sinusoids in a pattern similar to ICAM-1 staining. PECAM-1 specific transcripts were detected in freshly isolated and cultured SECs. After a single CCl4-administration, PECAM-1 immunoreactivity did not increase along the sinusoids in contrast to the early increase of ICAM-1. Northern blot analysis indicated that PECAM-1 expression in liver tissue and in isolated SECs does not increase after a single administration of CCl4, whereas ICAM-1 steady-state level increased after 6 h. In diseased human livers PECAM-1 was detectable along the sinusoids, within inflammatory infiltrates and within fibrotic septa. Neither in acutely nor chronically diseased human livers was an obvious increase of PECAM-1 immunoreactivity detectable.
  
  
  CONCLUSIONS
  PECAM-1 is expressed by SECs. In contrast to ICAM-1, PECAM-1 transcript level is not enhanced during liver damage.
authors.affiliation: University of Göttingen, Department of Internal Medicine, Section of Gastroenterology and Endocrinology, Germany.
authors.forename: K
authors.initials: K
authors.lastname: Neubauer
authors.forename: T
authors.initials: T
authors.lastname: Wilfling
authors.forename: A
authors.initials: A
authors.lastname: Ritzel
authors.forename: G
authors.initials: G
authors.lastname: Ramadori
mesh_terms: D000818:Animals; D002251:Carbon Tetrachloride; D056486:Chemical and Drug Induced Liver Injury; D004730:Endothelium, Vascular / Q000473:pathology / Q000503:physiopathology*; D015870:Gene Expression; D006801:Humans; D007158:Immunologic Techniques; D017403:In Situ Hybridization; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism; D008102:Liver Circulation; D008107:Liver Diseases / Q000235:genetics / Q000473:pathology / Q000503:physiopathology*; D008115:Liver Regeneration / Q000235:genetics*; D008297:Male; D008854:Microscopy, Electron; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000235:genetics* / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012016:Reference Values
chemical_list: D019408:Platelet Endothelial Cell Adhesion Molecule-1; D012333:RNA, Messenger; D018799:Intercellular Adhesion Molecule-1; D002251:Carbon Tetrachloride