title: Augmented damage of islets by impaired exocrine acinar cells undergoing apoptosis that is possibly converted to necrosis during isolation.
abstract: Islet damage attributed to impaired exocrine cells during pancreas preservation and isolation procedure remains elusive, although released exocrine enzymes could directly damage islets. The aim of this study is to investigate the cellular mechanisms associated with exocrine cells and their possible impact on the islet cell survival and function after isolation. Mouse pancreata were stored in cold University of Wisconsin preservation solution for 0, 24 and 48 h and incubated with or without collagenase at 37°C for 15 min. During preservation, the percentage of exocrine cells with necrosis, which means impaired cellular membrane that allows intracellular enzymes to be released, remains low (< 10%) regardless of preservation time; whereas the percentage of exocrine cells with apoptosis, which means impaired nucleus and possible intact cellular membrane, increases over time of preservation. After collagenase-free incubation, however, the percentage of exocrine cells with necrosis became higher in longer preservation time, and more than 60% of the necrotic exocrine cells contained apoptosis as well. Islet cells located in pancreata with intact structure are almost kept away either from necrotic or apoptotic changes even after 48 h preservation followed by collagenase-free incubation. However, when islets are isolated after collagenase-containing incubation, the percentage of islet cells with necrosis increases over time of preservation up to approximately 40%. This study suggests that exocrine cells with necrosis could cause damage of isolated islets when the pancreas is dissociated and that the necrosis in exocrine cells might be induced mainly as the conversion from apoptosis that has already existed during preservation.
authors.affiliation: Department of Anestesia, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
authors.forename: Hamed
authors.initials: H
authors.lastname: Elgendy
authors.forename: Teru
authors.initials: T
authors.lastname: Okitsu
authors.forename: Yasuko
authors.initials: Y
authors.lastname: Kimura
authors.forename: Xibao
authors.initials: X
authors.lastname: Liu
authors.forename: Hanaa
authors.initials: H
authors.lastname: Nafady-Hego
authors.forename: Jiro
authors.initials: J
authors.lastname: Kurata
authors.forename: Hiroki
authors.initials: H
authors.lastname: Teramae
authors.forename: Ashraf
authors.initials: A
authors.lastname: Elbahrawy
authors.forename: Shinji
authors.initials: S
authors.lastname: Uemoto
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Fukuda
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D002470:Cell Survival / Q000187:drug effects / Q000502:physiology; D017364:Collagenases / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism / Q000473:pathology / Q000601:surgery; D006651:Histocytochemistry; D020287:In Situ Nick-End Labeling; D007515:Islets of Langerhans / Q000166:cytology* / Q000473:pathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D019188:Organ Preservation Solutions / Q000378:metabolism*; D013047:Specific Pathogen-Free Organisms
chemical_list: D019188:Organ Preservation Solutions; D017364:Collagenases