title: Impact of hyperglycemia and acute pancreatitis on the receptor for advanced glycation endproducts.
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.
authors.affiliation: Institute for Experimental Surgery, University of Rostock Schillingallee 69a, 18057 Rostock, Germany.
authors.forename: Dietmar
authors.initials: D
authors.lastname: Zechner
authors.forename: Kai
authors.initials: K
authors.lastname: Sempert
authors.forename: Berit
authors.initials: B
authors.lastname: Genz
authors.forename: Franziska
authors.initials: F
authors.lastname: Timm
authors.forename: Florian
authors.initials: F
authors.lastname: Bürtin
authors.forename: Tim
authors.initials: T
authors.lastname: Kroemer
authors.forename: Antje
authors.initials: A
authors.lastname: Butschkau
authors.forename: Angela
authors.initials: A
authors.lastname: Kuhla
authors.forename: Brigitte
authors.initials: B
authors.lastname: Vollmar
mesh_terms: D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism* / Q000473:pathology; D018450:Disease Progression; D006943:Hyperglycemia / Q000378:metabolism* / Q000473:pathology; D008049:Lipase / Q000378:metabolism; D020935:MAP Kinase Signaling System / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D010179:Pancreas / Q000378:metabolism* / Q000473:pathology; D010195:Pancreatitis / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D010766:Phosphorylation; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic / Q000378:metabolism*
chemical_list: D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic; D008049:Lipase
keywords: ERK1/ERK2 phosphorylation; Receptor for advanced glycation endproducts (RAGE) isoforms; hyperglycemia; inflammation; pancreatitis; soluble RAGE