title: Dissociation and reassembly of adherens junctions during experimental acute pancreatitis.
abstract: OBJECTIVE
  The initial pathophysiological events that characterize acute pancreatitis include the formation of pancreatic edema. An interstitial accumulation of fluid, however, is incompatible with the presence of intact intercellular junctions between acinar cells. This study examined the major components of adherens junctions, E-cadherin, alpha-catenin, beta-catenin, and actin, during the initial phase of experimental pancreatitis.
  
  
  METHODS
  Pancreatitis was induced in rats by 10 micrograms.kg-1.h-1 intravenous cerulein for up to 12 hours. Adherens junction proteins were localized by immunocytochemistry for fluorescence microscopy or electron microscopy, their expression was studied by slot blot analysis, and their association was investigated by immunoprecipitation and Western blot.
  
  
  RESULTS
  During a rapid increase of E-cadherin-encoding RNA, E-cadherin protein declined only moderately and, unlike its cytoskeletal binding partner actin, was not proteolytically cleaved during pancreatitis. Morphologically, E-cadherin and beta-catenin were localized at the basolateral cell membrane from where they rapidly dissociated early in pancreatitis and to where they slowly relocalized during the subsequent course. E-cadherin/beta-catenin complexes disintegrated and reassembled completely in parallel on immunoprecipitation experiments.
  
  
  CONCLUSIONS
  The dissociation of adherens junctions and the internalization, relocalization, and reassembly of their major components seem to represent the critical biochemical event at cell-cell contacts during edema formation and resolution in acute pancreatitis.
authors.affiliation: Department of Internal Medicine I, Ulm University, Germany.
authors.forename: M M
authors.initials: MM
authors.lastname: Lerch
authors.forename: M P
authors.initials: MP
authors.lastname: Lutz
authors.forename: H
authors.initials: H
authors.lastname: Weidenbach
authors.forename: F
authors.initials: F
authors.lastname: Müller-Pillasch
authors.forename: T M
authors.initials: TM
authors.lastname: Gress
authors.forename: J
authors.initials: J
authors.lastname: Leser
authors.forename: G
authors.initials: G
authors.lastname: Adler
mesh_terms: D000199:Actins / Q000032:analysis; D000208:Acute Disease; D000818:Animals; D015820:Cadherins / Q000032:analysis* / Q000096:biosynthesis; D002108:Ceruletide; D003598:Cytoskeletal Proteins / Q000032:analysis* / Q000096:biosynthesis; D007365:Intercellular Junctions / Q000473:pathology* / Q000502:physiology* / Q000648:ultrastructure; D008297:Male; D010179:Pancreas / Q000473:pathology* / Q000503:physiopathology / Q000648:ultrastructure; D010195:Pancreatitis / Q000473:pathology* / Q000503:physiopathology*; D051381:Rats; D017208:Rats, Wistar; D015534:Trans-Activators; D051178:alpha Catenin; D051176:beta Catenin
chemical_list: D000199:Actins; D015820:Cadherins; C495268:Ctnnb1 protein, rat; D003598:Cytoskeletal Proteins; D015534:Trans-Activators; D051178:alpha Catenin; D051176:beta Catenin; D002108:Ceruletide