PMID- 18538757 OWN - NLM STAT- MEDLINE DCOM- 20081031 LR - 20161124 IS - 1090-2392 (Electronic) IS - 0011-2240 (Linking) VI - 57 IP - 1 DP - 2008 Aug TI - Prevention of cold ischemia/rewarming-induced ERK 1/2, p38 kinase and HO-1 activation by trophic factor supplementation of UW solution. PG - 72-4 LID - 10.1016/j.cryobiol.2008.04.003 [doi] AB - We have previously shown that trophic factor supplementation (TFS) of University of Wisconsin (UW) solution reduced early apoptotic changes in vascular endothelial cells. Here, we examine the effect of TFS on cell signaling pathways related to cell growth, differentiation, and apoptosis after cold ischemic storage. In this study, the effect of TFS on the phosphorylation of signaling molecules ERK (extracellular regulated-signaling kinase) 1/2 and p38 MAPK (mitogen activated protein kinases) and of HO-1 (hemeoxygenase-1), relative to changes seen in unmodified UW solution, were determined by Western blot in cells stored under cold ischemic conditions. Primary cultures of canine kidney proximal tubule cells (CKPTC) and human umbilical vein endothelial cells (HUVEC) were used in this study. There was a significant decrease, relative to UW solution, after 1 min rewarming in ERK 1 and 2 activity in CKPTCs. For p38 MAPK, a significant decrease after 5 min rewarming was seen in CKPTC (p<0.05) while significant reductions relative to UW solution were seen in HUVECs after both 1 and 5 min rewarming (p<0.05). Phosphorylated HO-1 was also decreased by 43% and 50% in HUVECs, relative to UW solution, after 1 and 5 min rewarming (p<0.05 at each time point). Collectively, TFS not only limits ERK 1/2 and p38 MAPK activity induced by cold ischemic injury and subsequent rewarming, but also substantially restricted increases in HO-1 phosphorylation. FAU - Kwon, Young Sam AU - Kwon YS AD - Department of Surgical Sciences, School of Veterinary Medicine, University of Wisconsin, 2015 Linden Drive W, Madison, WI 53706-1102, USA. FAU - Foley, John D AU - Foley JD FAU - Russell, Paul AU - Russell P FAU - McAnulty, Jonathan F AU - McAnulty JF FAU - Murphy, Christopher J AU - Murphy CJ LA - eng PT - Journal Article DEP - 20080425 PL - Netherlands TA - Cryobiology JT - Cryobiology JID - 0006252 RN - 0 (Insulin) RN - 0 (Intercellular Signaling Peptides and Proteins) RN - 0 (Organ Preservation Solutions) RN - 0 (University of Wisconsin-lactobionate solution) RN - 63CZ7GJN5I (Allopurinol) RN - EC 1.14.14.18 (Heme Oxygenase-1) RN - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases) RN - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1) RN - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3) RN - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases) RN - GAN16C9B8O (Glutathione) RN - K72T3FS567 (Adenosine) RN - N5O3QU595M (Raffinose) SB - IM MH - Adenosine/metabolism/pharmacology MH - Allopurinol/metabolism/pharmacology MH - Animals MH - Apoptosis MH - Cells, Cultured MH - *Cold Ischemia MH - Dogs MH - Extracellular Signal-Regulated MAP Kinases/*metabolism MH - Glutathione/metabolism/pharmacology MH - Heme Oxygenase-1/*metabolism MH - Humans MH - Insulin/metabolism/pharmacology MH - Intercellular Signaling Peptides and Proteins/pharmacology MH - Kidney Tubules/cytology/drug effects MH - Mitogen-Activated Protein Kinase 1/metabolism MH - Mitogen-Activated Protein Kinase 3/metabolism MH - Organ Preservation Solutions/metabolism/*pharmacology MH - Phosphorylation MH - Raffinose/metabolism/pharmacology MH - Signal Transduction MH - Wisconsin MH - p38 Mitogen-Activated Protein Kinases/*metabolism EDAT- 2008/06/10 09:00 MHDA- 2008/11/01 09:00 CRDT- 2008/06/10 09:00 PHST- 2007/11/24 00:00 [received] PHST- 2008/04/05 00:00 [revised] PHST- 2008/04/07 00:00 [accepted] PHST- 2008/06/10 09:00 [pubmed] PHST- 2008/11/01 09:00 [medline] PHST- 2008/06/10 09:00 [entrez] AID - S0011-2240(08)00053-9 [pii] AID - 10.1016/j.cryobiol.2008.04.003 [doi] PST - ppublish SO - Cryobiology. 2008 Aug;57(1):72-4. doi: 10.1016/j.cryobiol.2008.04.003. Epub 2008 Apr 25.