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Int J Clin Exp Pathol 2013;6(10):2021-2029
Impact of hyperglycemia and acute pancreatitis on the receptor for advanced glycation
Dietmar Zechner, Kai Sempert, Berit Genz, Franziska Timm, Florian Bürtin, Tim Kroemer, Antje Butschkau, Angela Kuhla, Brigitte Vollmar
Institute for Experimental Surgery, University of Rostock, Schillingallee 69a, 18057 Rostock, Germany. Equal contributors.
Received August 14, 2013; Accepted August 29, 2013; Epub September 15, 2013; Published October 1, 2013
Abstract: Since hyperglycemia aggravates acute pancreatitis and also activates the receptor for advanced glycation endproducts (RAGE) in
other organs, we explored if RAGE is expressed in the pancreas and if its expression is regulated during acute pancreatitis and hyperglycemia.
Acute pancreatitis was induced by cerulein in untreated and streptozotocin treated diabetic mice. Expression of RAGE was analyzed by Western
blot and immunohistochemistry. To evaluate signal transduction the phosphorylation of ERK1/ERK2 was assessed by Western blot and the
progression of acute pancreatitis was monitored by evaluation of lipase activity and the pancreas wet to dry weight ratio. RAGE is mainly
expressed by acinar as well as interstitial cells in the pancreas. During acute pancreatitis infiltrating inflammatory cells also express RAGE.
Using two distinct anti-RAGE antibodies six RAGE proteins with diverse molecular weight are detected in the pancreas, whereas just three
distinct RAGE proteins are detected in the lung. Hyperglycemia, which aggravates acute pancreatitis, significantly reduces the production of two
RAGE proteins in the inflamed pancreas. (IJCEP1308036).
Keywords: Receptor for advanced glycation endproducts (RAGE) isoforms, soluble RAGE, pancreatitis, hyperglycemia, inflammation,
Address correspondence to: Dr. Dietmar Zechner, Institute for Experimental Surgery, University of Rostock, Schillingallee 69a, 18057 Rostock,
Germany. Tel: +49 381 494 2512; Fax: +49 381 494 2502; E-mail: firstname.lastname@example.org