title: Pancreatic regenerating protein (reg I) and reg I receptor mRNA are upregulated in rat pancreas after induction of acute pancreatitis.
abstract: OBJECTIVE
  Pancreatic regenerating protein (reg I) stimulates pancreatic regeneration after pancreatectomy and is mitogenic to ductal and beta-cells. This suggests that reg I and its receptor may play a role in recovery after pancreatic injury. We hypothesized that reg I and its receptor are induced in acute pancreatitis.
  
  
  METHODS
  Acute pancreatitis was induced in male Wistar rats by retrograde injection of 3% sodium taurocholate into the pancreatic duct. Pancreata and serum were collected 12, 24, and 36 h after injection and from normal controls (4 rats/group). Reg I receptor mRNA, serum reg I protein, and tissue reg I protein levels were determined by Northern analysis, enzyme-linked immunosorbent assay (ELISA), and Western analysis, respectively. Immunohistochemistry was used to localize changes in reg I and its receptor.
  
  
  RESULTS
  Serum amylase levels and histology confirmed necrotizing pancreatitis in taurocholate treated rats. There was no statistically significant change in serum reg I concentrations from controls. However, Western blot demonstrated increased tissue levels of reg I at 24 and 36 h. This increase was localized primarily to the acinar cells and the ductal cells by immunohistochemistry. Northern blot demonstrated a significant increase in reg I receptor mRNA expression with pancreatitis. Immunohistochemistry localized this increase to the ductal cells, islets, and acinar cells.
  
  
  CONCLUSIONS
  Acute pancreatitis results in increased tissue reg I protein levels localized to the acinar and ductal cells, and a parallel threefold induction of reg I receptor in the ductal cells, islets, and acinar cells. These changes suggest that induction of reg I and its receptor may be important for recovery from acute pancreatitis.
authors.affiliation: Department of Surgery, State University of New York-Downstate Medical Center, Brooklyn, New York, USA. michael.zenilman@downstate.edu
authors.forename: Martin H
authors.initials: MH
authors.lastname: Bluth
authors.forename: Sameer A
authors.initials: SA
authors.lastname: Patel
authors.forename: Brian K
authors.initials: BK
authors.lastname: Dieckgraefe
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Okamoto
authors.forename: Michael E
authors.initials: ME
authors.lastname: Zenilman
mesh_terms: D000681:Amylases / Q000097:blood; D000818:Animals; D002454:Cell Differentiation; D049109:Cell Proliferation; D005786:Gene Expression Regulation; D051847:Lithostathine / Q000235:genetics* / Q000378:metabolism; D008297:Male; D010179:Pancreas / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D019283:Pancreatitis, Acute Necrotizing / Q000139:chemically induced / Q000235:genetics* / Q000378:metabolism* / Q000473:pathology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D011956:Receptors, Cell Surface / Q000235:genetics* / Q000378:metabolism; D012038:Regeneration / Q000502:physiology; D013656:Taurocholic Acid
chemical_list: D051847:Lithostathine; C514404:REG I receptor, rat; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; C497616:Reg1a protein, rat; D013656:Taurocholic Acid; D000681:Amylases