Pancreatic regenerating protein (reg I) and reg I receptor mRNA are upregulated in rat pancreas after induction of acute panceatitis

Martin H. Bluth, Sameer A. Patel, Brian K. Dieckgraefe, Hiroshi Okamoto, Michael E. Zenilman

Research output: Contribution to journalArticle

Abstract

Aim: Pancreatic regenerating protein (reg I ) stimulates pancreatic regeneration after pancreatectomy and is mitogenic to ductal and β-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 a male Wistar rats by retrograde injection of 3% sodium taurocholate into the pancreatic duct. Pancreata and serum were collected 12, 24, and 36 hours 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. Conclusion: 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.

Original languageEnglish (US)
Pages (from-to)4511-4516
Number of pages6
JournalWorld Journal of Gastroenterology
Volume12
Issue number28
StatePublished - Jul 28 2006
Externally publishedYes

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Pancreas
Messenger RNA
Pancreatitis
Proteins
Acinar Cells
Taurocholic Acid
Immunohistochemistry
Islets of Langerhans
Blood Proteins
Injections
Pancreatectomy
Pancreatic Ducts
Amylases
Serum
Northern Blotting
Wistar Rats
Regeneration
Histology
Western Blotting
Enzyme-Linked Immunosorbent Assay

Keywords

  • Acute pancreatitis
  • Reg, reg receptor
  • Regeneration
  • Taurocholate

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Bluth, M. H., Patel, S. A., Dieckgraefe, B. K., Okamoto, H., & Zenilman, M. E. (2006). Pancreatic regenerating protein (reg I) and reg I receptor mRNA are upregulated in rat pancreas after induction of acute panceatitis. World Journal of Gastroenterology, 12(28), 4511-4516.

Pancreatic regenerating protein (reg I) and reg I receptor mRNA are upregulated in rat pancreas after induction of acute panceatitis. / Bluth, Martin H.; Patel, Sameer A.; Dieckgraefe, Brian K.; Okamoto, Hiroshi; Zenilman, Michael E.

In: World Journal of Gastroenterology, Vol. 12, No. 28, 28.07.2006, p. 4511-4516.

Research output: Contribution to journalArticle

Bluth, Martin H. ; Patel, Sameer A. ; Dieckgraefe, Brian K. ; Okamoto, Hiroshi ; Zenilman, Michael E. / Pancreatic regenerating protein (reg I) and reg I receptor mRNA are upregulated in rat pancreas after induction of acute panceatitis. In: World Journal of Gastroenterology. 2006 ; Vol. 12, No. 28. pp. 4511-4516.
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abstract = "Aim: Pancreatic regenerating protein (reg I ) stimulates pancreatic regeneration after pancreatectomy and is mitogenic to ductal and β-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 a male Wistar rats by retrograde injection of 3{\%} sodium taurocholate into the pancreatic duct. Pancreata and serum were collected 12, 24, and 36 hours 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. Conclusion: 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.",
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