The effect of trophic factor supplementation on cold ischemia-induced early apoptotic changes

• Published in: Transplantation Vol. 83; no. 1; p. 91
• Main Authors: Kwon, Young Sam, Foley, John D, Murphy, Christopher J, McAnulty, Jonathan F
• Format: Journal Article
• Language: English
• Published: United States 15.01.2007
• Subjects: Animals; Apoptosis - drug effects; Cell Line; Dietary Supplements; Dogs; Humans; Intercellular Signaling Peptides and Proteins - pharmacology; Ischemia; Kidney - cytology; Kidney - drug effects; Kidney - physiology; Kidney Tubules - cytology; Kidney Tubules - drug effects; Kidney Tubules - physiology; Membrane Potentials - drug effects; Membrane Potentials - physiology; Mitochondria - drug effects; Mitochondria - physiology; Umbilical Veins - cytology; Umbilical Veins - drug effects; Umbilical Veins - physiology
• ISSN: 0041-1337
• DOI: 10.1097/01.tp.0000242524.35562.4b

We have previously shown that trophic factor supplementation (TFS) of University of Wisconsin (UW) solution enhanced kidney viability after cold storage. Here, we use an in vitro model to study the effect of TFS on early apoptotic changes after cold ischemic storage. Mitochondrial membrane potential was determined by fluorescence intensity in primary canine kidney tubule cells, Madin-Darby canine kidney cells, and human umbilical vein endothelial cells. In addition, caspase 3 enzyme activity assay and immunofluorescence staining were performed to evaluate apoptosis. There was a 15% increase in mitochondrial membrane potential in human umbilical vein endothelial cells stored in trophic factor supplemented University of Wisconsin solution after four-hour rewarming (P<0.05). TFS suppressed caspase 3 enzyme activity and activation in human umbilical vein endothelial cells. We confirmed that the presence of TFS in UW solution has a beneficial effect by protecting mitochondrial function and reducing early apoptotic changes in vascular endothelial cells.