title: Increased expression of transforming growth factor beta s after acute oedematous pancreatitis in rats suggests a role in pancreatic repair.
abstract: BACKGROUND
  Transforming growth factor beta isoforms (TGF beta s) belong to a family of multifunctional regulators of cellular growth and differentiation. They are mitogenic and chemotactic for fibroblasts and are potent stimulators of extracellular matrix production (collagen) and deposition. Upregulation of TGF beta transcription has been reported for several in vivo systems during repair after injury.
  
  
  OBJECTIVE
  To study the expression of the three mammalian isoforms of TGF beta (TGF beta 1-3) and their relation to collagen expression as a marker for fibroblast response in acute oedematous pancreatitis in rats.
  
  
  METHODS
  Using northern blot analysis and immunohistochemistry, the expression and localisation of TGF beta isoforms, collagen, and amylase were analysed during the course of acute oedematous pancreatitis in rats, experimentally induced by intravenous caerulein infusion.
  
  
  RESULTS
  Induction of acute pancreatitis resulted in a biphasic peak pattern of expression of TGF beta 1, beta 2, and beta 3 mRNA, with a pronounced increase from day 1 to day 3 (sixfold, 2.5-fold, fivefold, respectively) and again from day 5 to day 7 (three-fold, 2.3-fold, 3.5-fold, respectively). The temporal changes in TGF beta mRNA identically paralleled the expression in collagen mRNA. In contrast, amylase mRNA expression, used as a general indicator of acinar cell integrity, was slightly decreased after induction of acute pancreatitis. Immunohistochemical analysis of pancreatitis tissue showed that increased expression of TGF beta s was mainly present in the pancreatic acinar and ductal cells; this was evident within one day after pancreatitis induction.
  
  
  CONCLUSIONS
  Overexpression of TGF beta s after induction of acute pancreatitis suggests a role for these proteins in pancreatic repair and remodelling. The increased levels of TGF beta s may help suppress immune activation, and may contribute to the increase in the extracellular matrix including collagen and to the repair of the pancreatic parenchyma.
authors.affiliation: Department of Visceral and Transplantation Surgery, University of Bern, Inselspital, Switzerland.
authors.forename: E
authors.initials: E
authors.lastname: Riesle
authors.forename: H
authors.initials: H
authors.lastname: Friess
authors.forename: L
authors.initials: L
authors.lastname: Zhao
authors.forename: M
authors.initials: M
authors.lastname: Wagner
authors.forename: W
authors.initials: W
authors.lastname: Uhl
authors.forename: K
authors.initials: K
authors.lastname: Baczako
authors.forename: L I
authors.initials: LI
authors.lastname: Gold
authors.forename: M
authors.initials: M
authors.lastname: Korc
authors.forename: M W
authors.initials: MW
authors.lastname: Büchler
mesh_terms: D000208:Acute Disease; D000681:Amylases / Q000097:blood; D000818:Animals; D015152:Blotting, Northern; D002108:Ceruletide; D003094:Collagen / Q000032:analysis; D004487:Edema / Q000150:complications / Q000378:metabolism*; D005765:Gastrointestinal Agents; D015870:Gene Expression; D007150:Immunohistochemistry; D008297:Male; D010195:Pancreatitis / Q000139:chemically induced / Q000150:complications / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D016212:Transforming Growth Factor beta / Q000235:genetics / Q000378:metabolism*
chemical_list: D005765:Gastrointestinal Agents; D012333:RNA, Messenger; D016212:Transforming Growth Factor beta; D002108:Ceruletide; D003094:Collagen; D000681:Amylases