1. c-Jun N-terminal kinase 1 is deleterious to the function and survival of murine pancreatic islets
- Author
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Adeel Ijaz, M. Atsushi, Alessia Fornoni, R. D. Molano, J. L. Varona-Santos, Hirohito Ichii, Ricardo L. Pastori, Luca Inverardi, Nahir Y. Sanabria, Camillo Ricordi, and Antonello Pileggi
- Subjects
Male ,endocrine system ,medicine.medical_specialty ,endocrine system diseases ,Cell Survival ,Endocrinology, Diabetes and Metabolism ,medicine.medical_treatment ,MAPK8 ,Islets of Langerhans Transplantation ,Biology ,Diabetes Mellitus, Experimental ,Islets of Langerhans ,Mice ,chemistry.chemical_compound ,Internal medicine ,Internal Medicine ,medicine ,Animals ,Mitogen-Activated Protein Kinase 9 ,Mitogen-Activated Protein Kinase 8 ,Pancreatic islet function ,Phosphorylation ,Mice, Knockout ,geography ,geography.geographical_feature_category ,Pancreatic islets ,Graft Survival ,c-jun ,Islet ,Coculture Techniques ,Mice, Inbred C57BL ,Vascular endothelial growth factor ,Transplantation ,Endocrinology ,medicine.anatomical_structure ,Cytokine ,chemistry ,Cytokines - Abstract
Inhibition of c-jun N-terminal kinase (JNK) favours pancreatic islet function and survival. Since two JNK isoforms are present in the pancreas (JNK1 and JNK2), we addressed their specific roles in experimental islet transplantation. C57BL/6J (wild-type [WT]), Jnk1 (also known as Mapk8)−/− and Jnk2 (also known as Mapk9)−/− mice were used as donor/recipients in a syngeneic islet transplantation model. Islet cell composition, function, viability, production of cytokines and of vascular endothelial growth factor (VEGF) were also studied in vitro. Jnk1 −/− islets secreted more insulin in response to glucose and were more resistant to cytokine-induced cell death compared with WT and Jnk2 −/− islets (p
- Published
- 2008
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