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Scaffold-supported Transplantation of Islets in the Epididymal Fat Pad of Diabetic Mice
Published on: July 23, 2017
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Local Sphingosine Kinase 1 Activity Improves Islet Transplantation
Darling Rojas-Canales1,2, Daniella Penko1,2, Kay K Myo Min3
1Discipline of Medicine, The University of Adelaide, Adelaide, Australia.
Diabetes
|February 9, 2017
Summary
Sphingosine kinase 1 (SK1) is crucial for pancreatic islet transplantation success. SK1 deficiency impairs islet revascularization, leading to reduced graft function and diabetes cure in mice, highlighting SK1 as a therapeutic target.
Area of Science:
- Endocrinology
- Vascular Biology
- Transplantation Immunology
Background:
- Pancreatic islet transplantation is a key treatment for type 1 diabetes.
- Graft survival is limited by β-cell death and poor vascularization.
- The role of the sphingosine kinase (SK) pathway in islet transplantation is unknown.
Purpose of the Study:
- To investigate the role of sphingosine kinase 1 (SK1) in pancreatic islet survival and function after transplantation.
- To determine if SK1 is essential for revascularization of transplanted islets.
Main Methods:
- Utilized Sphingosine kinase 1 (SK1) knockout mice islets.
- Assessed intraislet vascularization and endothelial cell migration in vitro.
- Evaluated the efficacy of SK1-deficient islets in curing diabetes in vivo.
Main Results:
- SK1-deficient islets showed reduced resident vascular endothelial cells.
- Sphingosine-1-phosphate, the SK1 product, promoted endothelial cell migration in vitro.
- SK1-deficient islets exhibited impaired diabetes cure compared to wild-type islets in vivo.
Conclusions:
- SK1 is critical for islet revascularization post-transplantation.
- SK1 deficiency impairs the ability of transplanted islets to recruit new blood vessels.
- Targeting SK1 may represent a novel strategy to enhance pancreatic islet transplant outcomes.
