title: h-sgk serine-threonine protein kinase gene as transcriptional target of transforming growth factor beta in human intestine.
abstract: OBJECTIVE
  Recently, the immediate early gene h-sgk was cloned as a hypertonicity-induced gene from human hepatoma cells. The aim of this study was to localize h-sgk messenger RNA (mRNA) expression in normal and inflamed intestinal mucosa and to identify potential transcriptional regulators.
  
  
  METHODS
  h-sgk mRNA in small intestinal mucosa from healthy persons and patients with Crohn's disease was determined by in situ hybridization. Transcriptional regulation was studied by Northern blot analysis of total RNA isolated from cultured human Intestine 407, U937, and HepG2 cells.
  
  
  RESULTS
  In normal ileum, h-sgk mRNA was selectively localized to the apical villus enterocytes, whereas no staining was detected in crypt cells. In Crohn's disease, enterocytes of the crypts expressed h-sgk and abundant h-sgk positive inflammatory cells appeared in the lamina propria. Combined h-sgk in situ hybridization and immunohistochemical analysis of CD68 antigen expression identified a part of these cells as macrophages. In addition to spatial correlation of transforming growth factor (TGF)-beta1 protein and h-sgk mRNA expression, h-sgk transcription in human Intestine 407 and HepG2 cells as well as in U937 monocytes/macrophages was strongly induced by TGF-beta1 in vitro.
  
  
  CONCLUSIONS
  h-sgk expression in normal and inflamed intestinal mucosa may be regulated by TGF-beta1 and may contribute to the pleiotropic actions of TGF-beta1 in mucosal cell populations.
authors.affiliation: Institute of Physiology, University of Tübingen, Tübingen, Germany. florian.lang@uni-tuebingen.de
authors.forename: S
authors.initials: S
authors.lastname: Waldegger
authors.forename: K
authors.initials: K
authors.lastname: Klingel
authors.forename: P
authors.initials: P
authors.lastname: Barth
authors.forename: M
authors.initials: M
authors.lastname: Sauter
authors.forename: M L
authors.initials: ML
authors.lastname: Rfer
authors.forename: R
authors.initials: R
authors.lastname: Kandolf
authors.forename: F
authors.initials: F
authors.lastname: Lang
mesh_terms: D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D015152:Blotting, Northern; D000001:Calcimycin / Q000494:pharmacology; D002478:Cells, Cultured; D003424:Crohn Disease / Q000378:metabolism; D003513:Cycloheximide / Q000494:pharmacology; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D007082:Ileum / Q000276:immunology / Q000378:metabolism; D017874:Immediate-Early Proteins; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D007249:Inflammation / Q000378:metabolism; D007375:Interleukin-1 / Q000494:pharmacology; D007413:Intestinal Mucosa / Q000378:metabolism* / Q000473:pathology; D007476:Ionophores / Q000494:pharmacology; D009687:Nuclear Proteins; D010703:Phorbol Esters / Q000494:pharmacology; D017346:Protein Serine-Threonine Kinases / Q000235:genetics* / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D014158:Transcription, Genetic / Q000187:drug effects*; D016212:Transforming Growth Factor beta / Q000378:metabolism* / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D020298:U937 Cells; D000099184:Serum-Glucocorticoid Regulated Kinases; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D000001:Calcimycin; D003513:Cycloheximide; D017874:Immediate-Early Proteins; D007375:Interleukin-1; D007476:Ionophores; D009687:Nuclear Proteins; D010703:Phorbol Esters; D017346:Protein Serine-Threonine Kinases; D012333:RNA, Messenger; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha; D000099184:Serum-Glucocorticoid Regulated Kinases; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C008876:phorbol-12,13-didecanoate