İzole Edilmiş Sıçan Pankreas Adacık Hücrelerine in Vitro Trombospondinin Etkisi

Abstract

Pancreas islet cells are very sensitive to hypoxic stress because of having small amount of anti-oxidant enzyme. Loss of islet cell viability due to hipoxic damage decreases success of transplantation. Islet- endothelial co-culture prevents the cell death and improves the cell function. Furthermore, transplanted islets to portal system are also in close contact with the endothelial cells. Some of the endothelium derived substance improve the viability of islet cells and some of them cause negative effects. Thrombospondin(TSP) is a multifunctional substance that is released from islet endothelial cells and its effect on islet cell is not clear. The aim of this study is to investigate whether TSP, which is an endothelial factor, is effective on the islet cell’s viability and function. Isolated islet cells were divided into three groups: in the control group no substance were added to the normal culture medium. In ER stress generated group, 20 μg/ml tunicamycin (TUN) and in the third group 200pM thrombospondin (TSP) was added. Then groups were incubated for 24 hours. We measured islet cell viability with FDA/PI and cell function with glucose stimulation. We explored ER stress with western blot and oxidative stress parameters. We concluded that 200 pM TSP does not affect the cell viability but cause cell dysfunction. It did not appeare to come by endoplasmic reticulum stress or oxidative stress. According to the results, TSP may cause damage in different mechanisms like exocytosis in the islet cells. The results of this study may be supported with in vivo experiments, various doses of TSP and incubation periods. Additional studies are needed to clarify the cellular mechanisms that cause functional loss.