The Experts below are selected from a list of 114 Experts worldwide ranked by ideXlab platform

Jeremy Hughes - One of the best experts on this subject based on the ideXlab platform.

  • macrophage monocyte depletion by clodronate but not Diphtheria Toxin improves renal ischemia reperfusion injury in mice
    Kidney International, 2012
    Co-Authors: David A. Ferenbach, Tara A. Sheldrake, Kevin Dhaliwal, Tiina Kipari, Lorna Marson, David C. Kluth, Jeremy Hughes
    Abstract:

    The role of resident renal mononuclear phagocytes in acute kidney injury is controversial with experimental data suggesting both deleterious and protective functions. To help resolve this, we used mice transgenic for the human Diphtheria Toxin receptor under the control of the CD11b promoter and treated them with Diphtheria Toxin, or liposomal clodronate, or both to deplete monocyte/mononuclear phagocytes prior to renal ischemia/reperfusion injury. Although either system effectively depleted circulating monocytes and resident mononuclear phagocytes, depletion was most marked in Diphtheria Toxin–treated mice. Despite this, Diphtheria Toxin treatment did not protect from renal ischemia. In contrast, mice treated with clodronate exhibited reduced renal failure and acute tubular necrosis, suggesting key differences between these depletion strategies. Clodronate did not deplete CD206-positive renal macrophages and, unlike Diphtheria Toxin, left resident CD11c-positive cells unscathed while inducing dramatic apoptosis in hepatic and splenic mononuclear phagocyte populations. Abolition of the protected phenotype by administration of Diphtheria Toxin to clodronate-treated mice suggested that the protective effect of clodronate resulted from the presence of a cytoprotective intrarenal population of mononuclear phagocytes sensitive to Diphtheria Toxin–mediated ablation.

  • Macrophage/monocyte depletion by clodronate, but not Diphtheria Toxin, improves renal ischemia/reperfusion injury in mice.
    Kidney international, 2012
    Co-Authors: David A. Ferenbach, Tara A. Sheldrake, Kevin Dhaliwal, Tiina Kipari, Lorna Marson, David C. Kluth, Jeremy Hughes
    Abstract:

    The role of resident renal mononuclear phagocytes in acute kidney injury is controversial with experimental data suggesting both deleterious and protective functions. To help resolve this, we used mice transgenic for the human Diphtheria Toxin receptor under the control of the CD11b promoter and treated them with Diphtheria Toxin, or liposomal clodronate, or both to deplete monocyte/mononuclear phagocytes prior to renal ischemia/reperfusion injury. Although either system effectively depleted circulating monocytes and resident mononuclear phagocytes, depletion was most marked in Diphtheria Toxin–treated mice. Despite this, Diphtheria Toxin treatment did not protect from renal ischemia. In contrast, mice treated with clodronate exhibited reduced renal failure and acute tubular necrosis, suggesting key differences between these depletion strategies. Clodronate did not deplete CD206-positive renal macrophages and, unlike Diphtheria Toxin, left resident CD11c-positive cells unscathed while inducing dramatic apoptosis in hepatic and splenic mononuclear phagocyte populations. Abolition of the protected phenotype by administration of Diphtheria Toxin to clodronate-treated mice suggested that the protective effect of clodronate resulted from the presence of a cytoprotective intrarenal population of mononuclear phagocytes sensitive to Diphtheria Toxin–mediated ablation.

David A. Ferenbach - One of the best experts on this subject based on the ideXlab platform.

  • macrophage monocyte depletion by clodronate but not Diphtheria Toxin improves renal ischemia reperfusion injury in mice
    Kidney International, 2012
    Co-Authors: David A. Ferenbach, Tara A. Sheldrake, Kevin Dhaliwal, Tiina Kipari, Lorna Marson, David C. Kluth, Jeremy Hughes
    Abstract:

    The role of resident renal mononuclear phagocytes in acute kidney injury is controversial with experimental data suggesting both deleterious and protective functions. To help resolve this, we used mice transgenic for the human Diphtheria Toxin receptor under the control of the CD11b promoter and treated them with Diphtheria Toxin, or liposomal clodronate, or both to deplete monocyte/mononuclear phagocytes prior to renal ischemia/reperfusion injury. Although either system effectively depleted circulating monocytes and resident mononuclear phagocytes, depletion was most marked in Diphtheria Toxin–treated mice. Despite this, Diphtheria Toxin treatment did not protect from renal ischemia. In contrast, mice treated with clodronate exhibited reduced renal failure and acute tubular necrosis, suggesting key differences between these depletion strategies. Clodronate did not deplete CD206-positive renal macrophages and, unlike Diphtheria Toxin, left resident CD11c-positive cells unscathed while inducing dramatic apoptosis in hepatic and splenic mononuclear phagocyte populations. Abolition of the protected phenotype by administration of Diphtheria Toxin to clodronate-treated mice suggested that the protective effect of clodronate resulted from the presence of a cytoprotective intrarenal population of mononuclear phagocytes sensitive to Diphtheria Toxin–mediated ablation.

  • Macrophage/monocyte depletion by clodronate, but not Diphtheria Toxin, improves renal ischemia/reperfusion injury in mice.
    Kidney international, 2012
    Co-Authors: David A. Ferenbach, Tara A. Sheldrake, Kevin Dhaliwal, Tiina Kipari, Lorna Marson, David C. Kluth, Jeremy Hughes
    Abstract:

    The role of resident renal mononuclear phagocytes in acute kidney injury is controversial with experimental data suggesting both deleterious and protective functions. To help resolve this, we used mice transgenic for the human Diphtheria Toxin receptor under the control of the CD11b promoter and treated them with Diphtheria Toxin, or liposomal clodronate, or both to deplete monocyte/mononuclear phagocytes prior to renal ischemia/reperfusion injury. Although either system effectively depleted circulating monocytes and resident mononuclear phagocytes, depletion was most marked in Diphtheria Toxin–treated mice. Despite this, Diphtheria Toxin treatment did not protect from renal ischemia. In contrast, mice treated with clodronate exhibited reduced renal failure and acute tubular necrosis, suggesting key differences between these depletion strategies. Clodronate did not deplete CD206-positive renal macrophages and, unlike Diphtheria Toxin, left resident CD11c-positive cells unscathed while inducing dramatic apoptosis in hepatic and splenic mononuclear phagocyte populations. Abolition of the protected phenotype by administration of Diphtheria Toxin to clodronate-treated mice suggested that the protective effect of clodronate resulted from the presence of a cytoprotective intrarenal population of mononuclear phagocytes sensitive to Diphtheria Toxin–mediated ablation.

Tiina Kipari - One of the best experts on this subject based on the ideXlab platform.

  • macrophage monocyte depletion by clodronate but not Diphtheria Toxin improves renal ischemia reperfusion injury in mice
    Kidney International, 2012
    Co-Authors: David A. Ferenbach, Tara A. Sheldrake, Kevin Dhaliwal, Tiina Kipari, Lorna Marson, David C. Kluth, Jeremy Hughes
    Abstract:

    The role of resident renal mononuclear phagocytes in acute kidney injury is controversial with experimental data suggesting both deleterious and protective functions. To help resolve this, we used mice transgenic for the human Diphtheria Toxin receptor under the control of the CD11b promoter and treated them with Diphtheria Toxin, or liposomal clodronate, or both to deplete monocyte/mononuclear phagocytes prior to renal ischemia/reperfusion injury. Although either system effectively depleted circulating monocytes and resident mononuclear phagocytes, depletion was most marked in Diphtheria Toxin–treated mice. Despite this, Diphtheria Toxin treatment did not protect from renal ischemia. In contrast, mice treated with clodronate exhibited reduced renal failure and acute tubular necrosis, suggesting key differences between these depletion strategies. Clodronate did not deplete CD206-positive renal macrophages and, unlike Diphtheria Toxin, left resident CD11c-positive cells unscathed while inducing dramatic apoptosis in hepatic and splenic mononuclear phagocyte populations. Abolition of the protected phenotype by administration of Diphtheria Toxin to clodronate-treated mice suggested that the protective effect of clodronate resulted from the presence of a cytoprotective intrarenal population of mononuclear phagocytes sensitive to Diphtheria Toxin–mediated ablation.

  • Macrophage/monocyte depletion by clodronate, but not Diphtheria Toxin, improves renal ischemia/reperfusion injury in mice.
    Kidney international, 2012
    Co-Authors: David A. Ferenbach, Tara A. Sheldrake, Kevin Dhaliwal, Tiina Kipari, Lorna Marson, David C. Kluth, Jeremy Hughes
    Abstract:

    The role of resident renal mononuclear phagocytes in acute kidney injury is controversial with experimental data suggesting both deleterious and protective functions. To help resolve this, we used mice transgenic for the human Diphtheria Toxin receptor under the control of the CD11b promoter and treated them with Diphtheria Toxin, or liposomal clodronate, or both to deplete monocyte/mononuclear phagocytes prior to renal ischemia/reperfusion injury. Although either system effectively depleted circulating monocytes and resident mononuclear phagocytes, depletion was most marked in Diphtheria Toxin–treated mice. Despite this, Diphtheria Toxin treatment did not protect from renal ischemia. In contrast, mice treated with clodronate exhibited reduced renal failure and acute tubular necrosis, suggesting key differences between these depletion strategies. Clodronate did not deplete CD206-positive renal macrophages and, unlike Diphtheria Toxin, left resident CD11c-positive cells unscathed while inducing dramatic apoptosis in hepatic and splenic mononuclear phagocyte populations. Abolition of the protected phenotype by administration of Diphtheria Toxin to clodronate-treated mice suggested that the protective effect of clodronate resulted from the presence of a cytoprotective intrarenal population of mononuclear phagocytes sensitive to Diphtheria Toxin–mediated ablation.

Kevin Dhaliwal - One of the best experts on this subject based on the ideXlab platform.

  • macrophage monocyte depletion by clodronate but not Diphtheria Toxin improves renal ischemia reperfusion injury in mice
    Kidney International, 2012
    Co-Authors: David A. Ferenbach, Tara A. Sheldrake, Kevin Dhaliwal, Tiina Kipari, Lorna Marson, David C. Kluth, Jeremy Hughes
    Abstract:

    The role of resident renal mononuclear phagocytes in acute kidney injury is controversial with experimental data suggesting both deleterious and protective functions. To help resolve this, we used mice transgenic for the human Diphtheria Toxin receptor under the control of the CD11b promoter and treated them with Diphtheria Toxin, or liposomal clodronate, or both to deplete monocyte/mononuclear phagocytes prior to renal ischemia/reperfusion injury. Although either system effectively depleted circulating monocytes and resident mononuclear phagocytes, depletion was most marked in Diphtheria Toxin–treated mice. Despite this, Diphtheria Toxin treatment did not protect from renal ischemia. In contrast, mice treated with clodronate exhibited reduced renal failure and acute tubular necrosis, suggesting key differences between these depletion strategies. Clodronate did not deplete CD206-positive renal macrophages and, unlike Diphtheria Toxin, left resident CD11c-positive cells unscathed while inducing dramatic apoptosis in hepatic and splenic mononuclear phagocyte populations. Abolition of the protected phenotype by administration of Diphtheria Toxin to clodronate-treated mice suggested that the protective effect of clodronate resulted from the presence of a cytoprotective intrarenal population of mononuclear phagocytes sensitive to Diphtheria Toxin–mediated ablation.

  • Macrophage/monocyte depletion by clodronate, but not Diphtheria Toxin, improves renal ischemia/reperfusion injury in mice.
    Kidney international, 2012
    Co-Authors: David A. Ferenbach, Tara A. Sheldrake, Kevin Dhaliwal, Tiina Kipari, Lorna Marson, David C. Kluth, Jeremy Hughes
    Abstract:

    The role of resident renal mononuclear phagocytes in acute kidney injury is controversial with experimental data suggesting both deleterious and protective functions. To help resolve this, we used mice transgenic for the human Diphtheria Toxin receptor under the control of the CD11b promoter and treated them with Diphtheria Toxin, or liposomal clodronate, or both to deplete monocyte/mononuclear phagocytes prior to renal ischemia/reperfusion injury. Although either system effectively depleted circulating monocytes and resident mononuclear phagocytes, depletion was most marked in Diphtheria Toxin–treated mice. Despite this, Diphtheria Toxin treatment did not protect from renal ischemia. In contrast, mice treated with clodronate exhibited reduced renal failure and acute tubular necrosis, suggesting key differences between these depletion strategies. Clodronate did not deplete CD206-positive renal macrophages and, unlike Diphtheria Toxin, left resident CD11c-positive cells unscathed while inducing dramatic apoptosis in hepatic and splenic mononuclear phagocyte populations. Abolition of the protected phenotype by administration of Diphtheria Toxin to clodronate-treated mice suggested that the protective effect of clodronate resulted from the presence of a cytoprotective intrarenal population of mononuclear phagocytes sensitive to Diphtheria Toxin–mediated ablation.

David C. Kluth - One of the best experts on this subject based on the ideXlab platform.

  • macrophage monocyte depletion by clodronate but not Diphtheria Toxin improves renal ischemia reperfusion injury in mice
    Kidney International, 2012
    Co-Authors: David A. Ferenbach, Tara A. Sheldrake, Kevin Dhaliwal, Tiina Kipari, Lorna Marson, David C. Kluth, Jeremy Hughes
    Abstract:

    The role of resident renal mononuclear phagocytes in acute kidney injury is controversial with experimental data suggesting both deleterious and protective functions. To help resolve this, we used mice transgenic for the human Diphtheria Toxin receptor under the control of the CD11b promoter and treated them with Diphtheria Toxin, or liposomal clodronate, or both to deplete monocyte/mononuclear phagocytes prior to renal ischemia/reperfusion injury. Although either system effectively depleted circulating monocytes and resident mononuclear phagocytes, depletion was most marked in Diphtheria Toxin–treated mice. Despite this, Diphtheria Toxin treatment did not protect from renal ischemia. In contrast, mice treated with clodronate exhibited reduced renal failure and acute tubular necrosis, suggesting key differences between these depletion strategies. Clodronate did not deplete CD206-positive renal macrophages and, unlike Diphtheria Toxin, left resident CD11c-positive cells unscathed while inducing dramatic apoptosis in hepatic and splenic mononuclear phagocyte populations. Abolition of the protected phenotype by administration of Diphtheria Toxin to clodronate-treated mice suggested that the protective effect of clodronate resulted from the presence of a cytoprotective intrarenal population of mononuclear phagocytes sensitive to Diphtheria Toxin–mediated ablation.

  • Macrophage/monocyte depletion by clodronate, but not Diphtheria Toxin, improves renal ischemia/reperfusion injury in mice.
    Kidney international, 2012
    Co-Authors: David A. Ferenbach, Tara A. Sheldrake, Kevin Dhaliwal, Tiina Kipari, Lorna Marson, David C. Kluth, Jeremy Hughes
    Abstract:

    The role of resident renal mononuclear phagocytes in acute kidney injury is controversial with experimental data suggesting both deleterious and protective functions. To help resolve this, we used mice transgenic for the human Diphtheria Toxin receptor under the control of the CD11b promoter and treated them with Diphtheria Toxin, or liposomal clodronate, or both to deplete monocyte/mononuclear phagocytes prior to renal ischemia/reperfusion injury. Although either system effectively depleted circulating monocytes and resident mononuclear phagocytes, depletion was most marked in Diphtheria Toxin–treated mice. Despite this, Diphtheria Toxin treatment did not protect from renal ischemia. In contrast, mice treated with clodronate exhibited reduced renal failure and acute tubular necrosis, suggesting key differences between these depletion strategies. Clodronate did not deplete CD206-positive renal macrophages and, unlike Diphtheria Toxin, left resident CD11c-positive cells unscathed while inducing dramatic apoptosis in hepatic and splenic mononuclear phagocyte populations. Abolition of the protected phenotype by administration of Diphtheria Toxin to clodronate-treated mice suggested that the protective effect of clodronate resulted from the presence of a cytoprotective intrarenal population of mononuclear phagocytes sensitive to Diphtheria Toxin–mediated ablation.