ArticleAnnals of surgery2001
Modulation of JNK and p38 stress activated protein kinases in isolated islets of Langerhans: insulin as an autocrine survival signal.
Article in Annals of surgery, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 51 citations in OpenAlex.
- The MEK Inhibitor Trametinib Suppresses Major Histocompatibility Antigen-mismatched Rejection Following Pancreatic Islet Transplantation.Transplantation direct · 2020Article
- Presence of diabetes autoantigens in extracellular vesicles derived from human islets.Scientific reports · 2017Article
- Islet Culture/Preservation Before Islet Transplantation.Cell medicine · 2015Review
- Inflammatory response in islet transplantation.International journal of endocrinology · 2014Review
- Ectopic expression of glucagon receptor in skeletal muscles improves glucose homeostasis in a mouse model of diabetes.Diabetologia · 2012Article
- 12-Lipoxygenase Products Reduce Insulin Secretion and {beta}-Cell Viability in Human Islets.The Journal of clinical endocrinology and metabolism · 2010Article
- Suppressor of cytokine signaling-1 inhibits caspase activation and protects from cytokine-induced beta cell death.Cellular and molecular life sciences : CMLS · 2009Article
- Article
- Pancreas preservation for pancreas and islet transplantation.Current opinion in organ transplantation · 2008Article
- Improvement of canine islet yield by donor pancreas infusion with a p38MAPK inhibitor.Transplantation · 2008Article
- Inhibition of c-jun N terminal kinase (JNK) improves functional beta cell mass in human islets and leads to AKT and glycogen synthase kinase-3 (GSK-3) phosphorylation.Diabetologia · 2008Article
- Insulin protects islets from apoptosis via Pdx1 and specific changes in the human islet proteome.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Autocrine insulin action activates Akt and increases survival of isolated human islets.Diabetologia · 2006Article
- Activation of 12-lipoxygenase in proinflammatory cytokine-mediated beta cell toxicity.Diabetologia · 2005Article
- Nicotinic acid-adenine dinucleotide phosphate-sensitive calcium stores initiate insulin signaling in human beta cells.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe objective of this study was to determine the effects of islet isolation and cytokine exposure on e-JUN NH2 terminal kinase (JNK) and p38 activation and whether insulin or the p38 inhibitor PD169316 could modify the response. SUMMARY BACKGROUND DATA: Islet transplantation exposes the cells of the graft to a variety of stressful stimuli that could promote beta-cell death and lead to graft failure.
methodsIslets from canine (n = 12) and cadaveric human (n = 6) pancreata were isolated and purified. Islets were cultured in CMRL 1066 with and without 100 ng/ml insulin. The response to cytokine stimulation with tumor necrosis factor (TNF)alpha and IL-1 beta and the p38 inhibitor PD169316 was also observed. Islet lysates were analyzed by Western blotting for total and phosphorylated JNK and p38 content. Apoptosis was assessed by TdT-mediated dUTP nick end labeling (TUNEL) assay and by a specific cell death enzyme-linked immunosorbant assay (ELISA).
resultsIn unstimulated islets, JNK activity was highest immediately following isolation, declining over 3 days to a low baseline level. The activity of p38 was lowest immediately after isolation, increasing progressively with time. The addition of insulin resulted in a more rapid decline in JNK activity, as opposed to p38, which showed no decrease in phosphorylation in response to insulin. In the cytokine stimulation studies, IL-1 beta stimulated p38 activation in a dose dependent manner, while JNK was relatively unaffected. PD169316 (100 microg/ml) was able to inhibit p38 activation in response to the isolation procedure as well as cytokine stimulation. Apoptotic activity was highest 24 hours after isolation, and was significantly reduced when islets were maintained in insulin-supplemented medium.
conclusionsInhibition of the stress-activated protein kinase (SAPK) pathways may be important for the maintenance of islet cell survival following islet isolation for transplantation. This study supports an autocrine role of insulin in this process.
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