The Experts below are selected from a list of 2316 Experts worldwide ranked by ideXlab platform
Thierry Hauet - One of the best experts on this subject based on the ideXlab platform.
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limitation of lipid peroxidation and Renal Medullary Cell injury of the kidney after 48 and 72 hour cold storage in university of wisconsin solution effect of trimetazidine
2000Co-Authors: J P Richer, H Gibelin, C Tallineau, Ben I Amor, William Hebrard, M Carretier, Thierry HauetAbstract:ISCHEMIA-reperfusion injury after organ transplantation is a major cause of delayed graft function. The pathogenesis of ischemia-reperfusion injury are well correlated with alterations in mitochondrial function, namely, decrease in ATP synthesis, NAD(P)H level, and mitochondrial membrane potential and generation of mitochondrial permeability transition. A previous study has demonstrated that the pretreatment with trimetazidine (TMZ) prevented these ischemia-reperfusion deleterious effects at both the Cellular and mitochondrial level. The aim of this study was to assess the effect of TMZ added to University of Wisconsin Solution (UW) during cold preservation in an isolated perfused pig kidney model against lipid peroxidation and Renal medulla damage. After cold preservation (CP), kidneys were perfused as previously described.
J P Richer - One of the best experts on this subject based on the ideXlab platform.
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limitation of lipid peroxidation and Renal Medullary Cell injury of the kidney after 48 and 72 hour cold storage in university of wisconsin solution effect of trimetazidine
2000Co-Authors: J P Richer, H Gibelin, C Tallineau, Ben I Amor, William Hebrard, M Carretier, Thierry HauetAbstract:ISCHEMIA-reperfusion injury after organ transplantation is a major cause of delayed graft function. The pathogenesis of ischemia-reperfusion injury are well correlated with alterations in mitochondrial function, namely, decrease in ATP synthesis, NAD(P)H level, and mitochondrial membrane potential and generation of mitochondrial permeability transition. A previous study has demonstrated that the pretreatment with trimetazidine (TMZ) prevented these ischemia-reperfusion deleterious effects at both the Cellular and mitochondrial level. The aim of this study was to assess the effect of TMZ added to University of Wisconsin Solution (UW) during cold preservation in an isolated perfused pig kidney model against lipid peroxidation and Renal medulla damage. After cold preservation (CP), kidneys were perfused as previously described.
Matthew D Breyer - One of the best experts on this subject based on the ideXlab platform.
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sirt1 activation protects the mouse Renal medulla from oxidative injury
2010Co-Authors: Yingying Wang, Mingzhi Zhang, Li You, Linda S Davis, Hong Fan, Haichun Yang, Agnes B Fogo, Roy Zent, Raymond C Harris, Matthew D BreyerAbstract:Sirtuin 1 (Sirt1) is a NAD+-dependent deacetylase that exerts many of the pleiotropic effects of oxidative metabolism. Due to local hypoxia and hypertonicity, the Renal medulla is subject to extreme oxidative stress. Here, we set out to investigate the role of Sirt1 in the kidney. Our initial analysis indicated that it was abundantly expressed in mouse Renal Medullary interstitial Cells in vivo. Knocking down Sirt1 expression in primary mouse Renal Medullary interstitial Cells substantially reduced Cellular resistance to oxidative stress, while pharmacologic Sirt1 activation using either resveratrol or SRT2183 improved Cell survival in response to oxidative stress. The unilateral ureteral obstruction (UUO) model of kidney injury induced markedly more Renal apoptosis and fibrosis in Sirt1+/- mice than in wild-type controls, while pharmacologic Sirt1 activation substantially attenuated apoptosis and fibrosis in wild-type mice. Moreover, Sirt1 deficiency attenuated oxidative stress-induced COX2 expression in cultured mouse Renal Medullary interstitial Cells, and Sirt1+/- mice displayed reduced UUO-induced COX2 expression in vivo. Conversely, Sirt1 activation increased Renal Medullary interstitial Cell COX2 expression both in vitro and in vivo. Furthermore, exogenous PGE2 markedly reduced apoptosis in Sirt1-deficient Renal Medullary interstitial Cells following oxidative stress. Taken together, these results identify Sirt1 as an important protective factor for mouse Renal Medullary interstitial Cells following oxidative stress and suggest that the protective function of Sirt1 is partly attributable to its regulation of COX2 induction. We therefore suggest that Sirt1 provides a potential therapeutic target to minimize Renal Medullary Cell damage following oxidative stress.
Ben I Amor - One of the best experts on this subject based on the ideXlab platform.
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limitation of lipid peroxidation and Renal Medullary Cell injury of the kidney after 48 and 72 hour cold storage in university of wisconsin solution effect of trimetazidine
2000Co-Authors: J P Richer, H Gibelin, C Tallineau, Ben I Amor, William Hebrard, M Carretier, Thierry HauetAbstract:ISCHEMIA-reperfusion injury after organ transplantation is a major cause of delayed graft function. The pathogenesis of ischemia-reperfusion injury are well correlated with alterations in mitochondrial function, namely, decrease in ATP synthesis, NAD(P)H level, and mitochondrial membrane potential and generation of mitochondrial permeability transition. A previous study has demonstrated that the pretreatment with trimetazidine (TMZ) prevented these ischemia-reperfusion deleterious effects at both the Cellular and mitochondrial level. The aim of this study was to assess the effect of TMZ added to University of Wisconsin Solution (UW) during cold preservation in an isolated perfused pig kidney model against lipid peroxidation and Renal medulla damage. After cold preservation (CP), kidneys were perfused as previously described.
William Hebrard - One of the best experts on this subject based on the ideXlab platform.
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limitation of lipid peroxidation and Renal Medullary Cell injury of the kidney after 48 and 72 hour cold storage in university of wisconsin solution effect of trimetazidine
2000Co-Authors: J P Richer, H Gibelin, C Tallineau, Ben I Amor, William Hebrard, M Carretier, Thierry HauetAbstract:ISCHEMIA-reperfusion injury after organ transplantation is a major cause of delayed graft function. The pathogenesis of ischemia-reperfusion injury are well correlated with alterations in mitochondrial function, namely, decrease in ATP synthesis, NAD(P)H level, and mitochondrial membrane potential and generation of mitochondrial permeability transition. A previous study has demonstrated that the pretreatment with trimetazidine (TMZ) prevented these ischemia-reperfusion deleterious effects at both the Cellular and mitochondrial level. The aim of this study was to assess the effect of TMZ added to University of Wisconsin Solution (UW) during cold preservation in an isolated perfused pig kidney model against lipid peroxidation and Renal medulla damage. After cold preservation (CP), kidneys were perfused as previously described.