Michael Lawrence
Baylor Scott & White Research Institute, USA
Title: Targeting pancreatic beta cell-derived isletokines to improve islet cell transplantation
Biography
Biography: Michael Lawrence
Abstract
Pancreatic islets are central to the regulation of glucose metabolism and homeostasis. The loss or impairment of islet beta cells results in diabetes and high risk of cardiovascular disease with detrimental health consequences. Islet cell transplantation represents a cell replacement therapy to prevent or reverse diabetes. One major hurdle to the success of islet transplantation is the early loss of islet cells due to an acute innate inflammatory response within the first 24 hours of islet cell infusion. We have identified cytokines and chemokines produced by beta cells that evoke acute islet inflammation. These “isletokines” are upregulated in stressed beta cells by calcineurin/NFAT and MAPK signaling and contribute to early islet cell graft loss. Here, we discuss our latest findings of key cellular events that induce beta cell isletokine expression and islet inflammation. We also identify molecular targets to prevent beta cell-induced islet inflammation and develop therapeutic strategies to improve islet cell transplantation.