Journal
ENDOCRINE JOURNAL
Volume 54, Issue 2, Pages 169-176Publisher
JAPAN ENDOCRINE SOC
DOI: 10.1507/endocrj.KR-87
Keywords
islet transplantation; c-jun NH2-terminal kinase; apoptosis; proinflammatory cytokine; protein transduction technology
Categories
Ask authors/readers for more resources
Pancreatic islet transplantation has been remarkably improved by the Edmonton protocol; however, it is not easy to achieve insulin independence after islet transplantation from one donor pancreas. The islet isolation procedure itself destroys cellular and noncellular components of the pancreas that probably play a role in supporting islet survival. Further islet transplantation exposes cells to a variety of stressful stimuli such as proinflammatory cytokines. The reduction in islet mass immediately after isolation and transplantation implicates P cell death by apoptosis and the prerecruitment of intracellular death signalling pathways. The c-Jun NH2-terminal kinases (JNKs) are classic stress-activated protein kinases and many cellular stresses have been shown to stimulate JNK activation. JNK in the pancreas is activated during brain death, pancreas procurement, and organ preservation, and its activity is progressively increased during the isolation procedure. Moreover, JNK activity in the transplanted liver after islet transplantation increases markedly within 24 hrs. Use of the JNK inhibitor in pancreas preservation, islet culture, and/or islet transplantation prevents islet apoptosis and improves islet graft function. These findings suggest that the control of JNK activation is important for pancreatic islet transplantation.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available