Document Detail


Augmented damage of islets by impaired exocrine acinar cells undergoing apoptosis that is possibly converted to necrosis during isolation.
MedLine Citation:
PMID:  21508665     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
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℃ 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:
Hamed Elgendy; Teru Okitsu; Yasuko Kimura; Xibao Liu; Hanaa Nafady-Hego; Jiro Kurata; Hiroki Teramae; Ashraf Elbahrawy; Shinji Uemoto; Kazuhiko Fukuda
Related Documents :
2336465 - Thermal tolerance during s phase for cell killing and chromosomal aberrations.
3175665 - Heat shock is lethal to fibroblasts microinjected with antibodies against hsp70.
6705795 - Mechanism of inhibition of polypeptide chain initiation in heat-shocked ehrlich ascites...
10089575 - Inhibition of nacl-induced heat shock protein 72 expression renders mdck cells suscepti...
11316565 - Differential expression of growth factors in irradiated mouse testes.
22770625 - Odontoblast-like mdpc-23 cells function as odontoclasts with the rankl/m-csf induction.
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-5-01
Journal Detail:
Title:  Islets     Volume:  3     ISSN:  1938-2022     ISO Abbreviation:  -     Publication Date:  2011 May 
Date Detail:
Created Date:  2011-4-21     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101495366     Medline TA:  Islets     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Affiliation:
Graduate School of Medicine; Kyoto University; Kyoto, Japan.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  MOLECULAR BACKGROUND AND GENOTYPE-PHENOTYPE CORRELATION IN APECED PATIENTS FROM CAMPANIA AND IN THEI...
Next Document:  Autophagy inhibition cooperates with erlotinib to induce glioblastoma cell death.