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Diabetes 51:994-999, 2002
© 2002 by the American Diabetes Association, Inc.

Carbon Monoxide Protects Pancreatic ß-Cells From Apoptosis and Improves Islet Function/Survival After Transplantation

Lukas Günther1, Pascal O. Berberat1, Manabu Haga1, Sophie Brouard3, R. Neal Smith2, Miguel P. Soares1, Fritz H. Bach1, and Edda Tobiasch1

1 Immunobiology Research Center, Department of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts
2 Immunopathology Unit, Department of Pathology, Massachusetts General Hospital, Boston, Massachusetts
3 INSERM U437, ITERT, Nantes, France

Pancreatic islets transplanted to treat autoimmune type 1 diabetes often fail to function (primary nonfunction), likely because of islet ß-cell apoptosis. We show that carbon monoxide (CO), a product of heme oxygenase activity, protects ß-cells from apoptosis. Protection is mediated through guanylate cyclase activation, generation of cyclic GMP (cGMP), and activation of cGMP-dependent protein kinases. This antiapoptotic effect is still observed when ß-cells are exposed to CO for 1 h before the apoptotic stimulus. In a similar manner, mouse islets exposed to CO for just 2 h function significantly better after transplantation than islets not exposed to CO. These findings suggest a potential therapeutic application for CO in improving islet function/survival after transplantation in humans.


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