Evaluation of Islet Transplantation from Non-Heart Beating Donors

Noguchi, Hirofumi; Iwanaga, Yasuhiro; Okitsu, Teru; Nagata, Hideo; Yonekawa, Yukihide; Matsumoto, Shinichi

doi:10.1111/j.1600-6143.2006.01499.x

Cited by 78 publications

(88 citation statements)

References 26 publications

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“…Application of the Edmonton protocol has markedly improved the outcome for pancreatic islet transplantation as a therapeutic strategy for type 1 diabetes [1][2][3]. However, the insulin independence rate after islet transplantation from one donor pancreas remains low.…”

Section: Introductionmentioning

confidence: 99%

Activation of c-Jun NH2-terminal kinase (JNK) pathway during islet transplantation and prevention of islet graft loss by intraportal injection of JNK inhibitor

Noguchi

Nakai

Ueda³

et al. 2007

Diabetologia

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Aims/hypothesis Although application of the Edmonton protocol has markedly improved the outcome for pancreatic islet transplantation, the insulin independence rate after islet transplantation from one donor pancreas has remained low. During the isolation process and subsequent clinical transplantation, islets are subjected to severe adverse conditions that impair survival and ultimately contribute to graft failure. The aim of this study was to map the c-Jun NH 2 -terminal kinase (JNK) pathway that mediates islet loss during islet transplantation and to clarify whether intraportal injection with JNK inhibitor during islet transplantation can prevent islet graft loss. Methods We measured JNK activity in the liver, fat and muscle of diabetic mice and in the liver immediately after islet transplantation. We examined the effect of intraportal injection of JNK inhibitory peptide at islet transplantation. Results JNK activity became progressively higher at least until 24 h after transplantation. The cell-permeable peptide of JNK inhibitor was delivered not only in the liver but also in other insulin target organs, preventing JNK activation in the liver at least until 24 h after transplantation and reducing JNK activity in these insulin target organs. Moreover, the peptide inhibitor prevented islet graft loss immediately after transplantation and improved islet transplant outcome. Conclusions/interpretation These findings suggest that control of the JNK pathway is extremely important in islet transplantation and that intraportal injection of JNK inhibitor during islet transplantation (addition of JNK inhibitor to transplant media) could prevent the impairment of islet cells, leading to improved outcome for pancreatic islet transplantation.

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Section: Introductionmentioning

confidence: 99%

Activation of c-Jun NH2-terminal kinase (JNK) pathway during islet transplantation and prevention of islet graft loss by intraportal injection of JNK inhibitor

Noguchi

Nakai

Ueda³

et al. 2007

Diabetologia

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“…Islet transplantation is an alternative method to whole pancreas transplantation in patients with type 1 diabetes because of its low invasiveness and safety for the recipient [68,69] . Significant progress in clinical islet transplantation has occurred during recent years, with a progressive improvement of short and long term outcomes.…”

Section: Resultsmentioning

confidence: 99%

Recent progress in pancreatic islet transplantation

Kubo

Noguchi²

2011

WJT

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“…The successes achieved over the last few decades with islet transplantation of whole pancreata and isolated islets suggest that diabetes can be cured by replenishing deficient β-cells [20,21]. It is logical that replacing the islet tissue itself is a better approach than simply replacing the lost insulin.…”

Section: Reversible Immortalized Pancreatic β-Cellsmentioning

confidence: 99%

Controlled Expansion of Mammalian Cell Populations by Reversible Immortalization

Noguchi¹,

Kobayashi²

2013

J Biotechnol Biomaterial

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In 1996, reversible immortalization using SV40 large T antigens and the Cre/LoxP system was successfully achieved with primary human fibroblasts. The concept of reversible immortalization involves introducing an immortalizing agent, SV40 large T antigens, into primary cells, expanding the cells in the culture, and finally, efficiently removing the immortalizing agent using Cre/LoxP site-specific recombination. The resulting cell population is essentially identical to the initial primary cells, but greatly increased in number. Since this report, reversible immortalization has been realized with hepatocytes, pancreatic β-cells, hepatic stellate cells, endothelial cells, renal epithelial cells and myogenic cells. This method facilitates the study of cell transplantation as well as cell differentiation, the cell cycle and senescence, by allowing one to control cell proliferation.

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Evaluation of Islet Transplantation from Non-Heart Beating Donors

Cited by 78 publications

References 26 publications

Activation of c-Jun NH2-terminal kinase (JNK) pathway during islet transplantation and prevention of islet graft loss by intraportal injection of JNK inhibitor

Activation of c-Jun NH2-terminal kinase (JNK) pathway during islet transplantation and prevention of islet graft loss by intraportal injection of JNK inhibitor

Recent progress in pancreatic islet transplantation

Controlled Expansion of Mammalian Cell Populations by Reversible Immortalization

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