作者: J Stagner , S Mokshagundam , K Wyler , E Samols , H Rilo
DOI: 10.1016/J.TRANSPROCEED.2004.04.036
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摘要: We have reported that vascular endothelial growth factor (VEGF) promotes the revascularization of transplanted islets, thereby reducing initial number required to prevent diabetes. The present study was undertaken assess other mechanisms beta-cell sparing by VEGF. For in vitro studies, islets were cultured for 14 days with versus without 20 ng/mL Viability, necrosis, and apoptosis examined specific staining (Alcein AM, propidium iodide, annexin/phosphatidylserine). effects VEGF on also a proteomic study. In vivo streptozotocin-treated diabetic Lewis rats received 1000 or Sprague-Dawley beneath renal capsule. Oxygen levels at transplant site monitored Clark-type oxygen electrode. Fasting blood glucose served as an indicator islet survival function. enhanced site. Syngeneic recipients euglycemic over 6 months, whereas control failed within 30 60 days. prevented allograft rejection days, controls rejected 7 Immunostaining suggested inhibited presentation MHC II antigen promoted inhibition necrosis apoptosis. Our preserved systems cellular preservation (heat shock proteins) insulin secretion. isolated variety mechanisms, including oxygenation immune rejection, provision exogenous may be useful adjunct transplantation.