The Experts below are selected from a list of 80043 Experts worldwide ranked by ideXlab platform
Sarah J Robertsthomson - One of the best experts on this subject based on the ideXlab platform.
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effects of peroxisome proliferator activated receptor γ ligands ciglitazone and 15 deoxy δ12 14 prostaglandin j2 on rat cultured cerebellar granule neuronal viability
Journal of Neuroscience Research, 2003Co-Authors: Steven A Smith, Jodie A Robinson, N. A. Holman, Gregory R. Monteith, Sarah J RobertsthomsonAbstract:Peroxisome proliferator-activated receptor gamma (PPARgamma) has been the focus of studies assessing its potential neuroprotective role. These studies have shown either Neuroprotection or neurotoxicity by PPARgamma ligands. Comparison of these studies is complicated by the use of different PPARgamma ligands, mechanisms of neurotoxicity induction, and neuronal cell type. In this study, we compared the effects of the synthetic PPARgamma ligand ciglitazone with an endogenous PPARgamma ligand, 15-deoxy-delta(12,14)-prostaglandin J(2) (15-deoxy PGJ(2)), on inherent neurotoxicity and Neuroprotection using a reduction in extracellular KCl in rat cultured cerebellar granule neurons (CGN). We also assessed the effects of these ligands on c-Jun protein expression, which is up-regulated on induction of low-KCl-mediated neuronal apoptosis as well as being associated with PPAR in other cell types. We showed that PPARgamma mRNA is expressed in CGN cultures and observed ciglitazone- and 15-deoxy PGJ(2)-mediated inherent neurotoxicity that was concentration and time dependent. c-Jun was only modestly increased in the presence of ciglitazone but was markedly up-regulated by 15-deoxy PGJ(2) after 12 hr. Treatment of CGN cultures with ciglitazone simultaneous with KCl withdrawal resulted in a modest, time-dependent Neuroprotection. Such Neuroprotection after KCl withdrawal was not observed with 15-deoxy PGJ(2). Despite the absence of Neuroprotection, 15-deoxy PGJ(2) markedly inhibited the early up-regulation of c-Jun during KCl withdrawal. These studies suggest that ciglitazone and 15-deoxy PGJ(2) have markedly different effects on inherent and low-KCl-induced toxicity and c-Jun expression in CGN, indicating potential non-PPARgamma mechanisms.
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effects of peroxisome proliferator activated receptor gamma ligands ciglitazone and 15 deoxy delta 12 14 prostaglandin j2 on rat cultured cerebellar granule neuronal viability steven a smith gregory r monteith nicola a holman jodie a robinson fiona j
Journal of Neuroscience Research, 2003Co-Authors: Steven A Smith, Jodie A Robinson, N. A. Holman, Gregory R. Monteith, Sarah J RobertsthomsonAbstract:Peroxisome proliferator-activated receptor (PPAR) has been the focus of studies assessing its potential neuroprotective role. These studies have shown either Neuroprotection or neurotoxicity by PPAR ligands. Comparison of these studies is complicated by the use of different PPAR ligands, mechanisms of neurotoxicity induction, and neuronal cell type. In this study, we compared the effects of the synthetic PPAR ligand ciglitazone with an endogenous PPAR ligand, 15-deoxy-12,14-prostaglandin J2 (15-deoxy PGJ2), on inherent neurotoxicity and Neuroprotection using a reduction in extracellular KCl in rat cultured cerebellar granule neurons (CGN). We also assessed the effects of these ligands on c-Jun protein expression, which is up-regulated on induction of low-KCl-mediated neuronal apoptosis as well as being associated with PPAR in other cell types. We showed that PPAR mRNA is expressed in CGN cultures and observed ciglitazone- and 15-deoxy PGJ2-mediated inherent neurotoxicity that was concentration and time dependent. c-Jun was only modestly increased in the presence of ciglitazone but was markedly up-regulated by 15-deoxy PGJ2 after 12 hr. Treatment of CGN cultures with ciglitazone simultaneous with KCl withdrawal resulted in a modest, time-dependent Neuroprotection. Such Neuroprotection after KCl withdrawal was not observed with 15-deoxy PGJ2. Despite the absence of Neuroprotection, 15-deoxy PGJ2 markedly inhibited the early up-regulation of c-Jun during KCl withdrawal. These studies suggest that ciglitazone and 15-deoxy PGJ2 have markedly different effects on inherent and low-KCl-induced toxicity and c-Jun expression in CGN, indicating potential non-PPAR mechanisms.
Steven A Smith - One of the best experts on this subject based on the ideXlab platform.
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effects of peroxisome proliferator activated receptor γ ligands ciglitazone and 15 deoxy δ12 14 prostaglandin j2 on rat cultured cerebellar granule neuronal viability
Journal of Neuroscience Research, 2003Co-Authors: Steven A Smith, Jodie A Robinson, N. A. Holman, Gregory R. Monteith, Sarah J RobertsthomsonAbstract:Peroxisome proliferator-activated receptor gamma (PPARgamma) has been the focus of studies assessing its potential neuroprotective role. These studies have shown either Neuroprotection or neurotoxicity by PPARgamma ligands. Comparison of these studies is complicated by the use of different PPARgamma ligands, mechanisms of neurotoxicity induction, and neuronal cell type. In this study, we compared the effects of the synthetic PPARgamma ligand ciglitazone with an endogenous PPARgamma ligand, 15-deoxy-delta(12,14)-prostaglandin J(2) (15-deoxy PGJ(2)), on inherent neurotoxicity and Neuroprotection using a reduction in extracellular KCl in rat cultured cerebellar granule neurons (CGN). We also assessed the effects of these ligands on c-Jun protein expression, which is up-regulated on induction of low-KCl-mediated neuronal apoptosis as well as being associated with PPAR in other cell types. We showed that PPARgamma mRNA is expressed in CGN cultures and observed ciglitazone- and 15-deoxy PGJ(2)-mediated inherent neurotoxicity that was concentration and time dependent. c-Jun was only modestly increased in the presence of ciglitazone but was markedly up-regulated by 15-deoxy PGJ(2) after 12 hr. Treatment of CGN cultures with ciglitazone simultaneous with KCl withdrawal resulted in a modest, time-dependent Neuroprotection. Such Neuroprotection after KCl withdrawal was not observed with 15-deoxy PGJ(2). Despite the absence of Neuroprotection, 15-deoxy PGJ(2) markedly inhibited the early up-regulation of c-Jun during KCl withdrawal. These studies suggest that ciglitazone and 15-deoxy PGJ(2) have markedly different effects on inherent and low-KCl-induced toxicity and c-Jun expression in CGN, indicating potential non-PPARgamma mechanisms.
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effects of peroxisome proliferator activated receptor gamma ligands ciglitazone and 15 deoxy delta 12 14 prostaglandin j2 on rat cultured cerebellar granule neuronal viability steven a smith gregory r monteith nicola a holman jodie a robinson fiona j
Journal of Neuroscience Research, 2003Co-Authors: Steven A Smith, Jodie A Robinson, N. A. Holman, Gregory R. Monteith, Sarah J RobertsthomsonAbstract:Peroxisome proliferator-activated receptor (PPAR) has been the focus of studies assessing its potential neuroprotective role. These studies have shown either Neuroprotection or neurotoxicity by PPAR ligands. Comparison of these studies is complicated by the use of different PPAR ligands, mechanisms of neurotoxicity induction, and neuronal cell type. In this study, we compared the effects of the synthetic PPAR ligand ciglitazone with an endogenous PPAR ligand, 15-deoxy-12,14-prostaglandin J2 (15-deoxy PGJ2), on inherent neurotoxicity and Neuroprotection using a reduction in extracellular KCl in rat cultured cerebellar granule neurons (CGN). We also assessed the effects of these ligands on c-Jun protein expression, which is up-regulated on induction of low-KCl-mediated neuronal apoptosis as well as being associated with PPAR in other cell types. We showed that PPAR mRNA is expressed in CGN cultures and observed ciglitazone- and 15-deoxy PGJ2-mediated inherent neurotoxicity that was concentration and time dependent. c-Jun was only modestly increased in the presence of ciglitazone but was markedly up-regulated by 15-deoxy PGJ2 after 12 hr. Treatment of CGN cultures with ciglitazone simultaneous with KCl withdrawal resulted in a modest, time-dependent Neuroprotection. Such Neuroprotection after KCl withdrawal was not observed with 15-deoxy PGJ2. Despite the absence of Neuroprotection, 15-deoxy PGJ2 markedly inhibited the early up-regulation of c-Jun during KCl withdrawal. These studies suggest that ciglitazone and 15-deoxy PGJ2 have markedly different effects on inherent and low-KCl-induced toxicity and c-Jun expression in CGN, indicating potential non-PPAR mechanisms.
Jodie A Robinson - One of the best experts on this subject based on the ideXlab platform.
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effects of peroxisome proliferator activated receptor γ ligands ciglitazone and 15 deoxy δ12 14 prostaglandin j2 on rat cultured cerebellar granule neuronal viability
Journal of Neuroscience Research, 2003Co-Authors: Steven A Smith, Jodie A Robinson, N. A. Holman, Gregory R. Monteith, Sarah J RobertsthomsonAbstract:Peroxisome proliferator-activated receptor gamma (PPARgamma) has been the focus of studies assessing its potential neuroprotective role. These studies have shown either Neuroprotection or neurotoxicity by PPARgamma ligands. Comparison of these studies is complicated by the use of different PPARgamma ligands, mechanisms of neurotoxicity induction, and neuronal cell type. In this study, we compared the effects of the synthetic PPARgamma ligand ciglitazone with an endogenous PPARgamma ligand, 15-deoxy-delta(12,14)-prostaglandin J(2) (15-deoxy PGJ(2)), on inherent neurotoxicity and Neuroprotection using a reduction in extracellular KCl in rat cultured cerebellar granule neurons (CGN). We also assessed the effects of these ligands on c-Jun protein expression, which is up-regulated on induction of low-KCl-mediated neuronal apoptosis as well as being associated with PPAR in other cell types. We showed that PPARgamma mRNA is expressed in CGN cultures and observed ciglitazone- and 15-deoxy PGJ(2)-mediated inherent neurotoxicity that was concentration and time dependent. c-Jun was only modestly increased in the presence of ciglitazone but was markedly up-regulated by 15-deoxy PGJ(2) after 12 hr. Treatment of CGN cultures with ciglitazone simultaneous with KCl withdrawal resulted in a modest, time-dependent Neuroprotection. Such Neuroprotection after KCl withdrawal was not observed with 15-deoxy PGJ(2). Despite the absence of Neuroprotection, 15-deoxy PGJ(2) markedly inhibited the early up-regulation of c-Jun during KCl withdrawal. These studies suggest that ciglitazone and 15-deoxy PGJ(2) have markedly different effects on inherent and low-KCl-induced toxicity and c-Jun expression in CGN, indicating potential non-PPARgamma mechanisms.
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effects of peroxisome proliferator activated receptor gamma ligands ciglitazone and 15 deoxy delta 12 14 prostaglandin j2 on rat cultured cerebellar granule neuronal viability steven a smith gregory r monteith nicola a holman jodie a robinson fiona j
Journal of Neuroscience Research, 2003Co-Authors: Steven A Smith, Jodie A Robinson, N. A. Holman, Gregory R. Monteith, Sarah J RobertsthomsonAbstract:Peroxisome proliferator-activated receptor (PPAR) has been the focus of studies assessing its potential neuroprotective role. These studies have shown either Neuroprotection or neurotoxicity by PPAR ligands. Comparison of these studies is complicated by the use of different PPAR ligands, mechanisms of neurotoxicity induction, and neuronal cell type. In this study, we compared the effects of the synthetic PPAR ligand ciglitazone with an endogenous PPAR ligand, 15-deoxy-12,14-prostaglandin J2 (15-deoxy PGJ2), on inherent neurotoxicity and Neuroprotection using a reduction in extracellular KCl in rat cultured cerebellar granule neurons (CGN). We also assessed the effects of these ligands on c-Jun protein expression, which is up-regulated on induction of low-KCl-mediated neuronal apoptosis as well as being associated with PPAR in other cell types. We showed that PPAR mRNA is expressed in CGN cultures and observed ciglitazone- and 15-deoxy PGJ2-mediated inherent neurotoxicity that was concentration and time dependent. c-Jun was only modestly increased in the presence of ciglitazone but was markedly up-regulated by 15-deoxy PGJ2 after 12 hr. Treatment of CGN cultures with ciglitazone simultaneous with KCl withdrawal resulted in a modest, time-dependent Neuroprotection. Such Neuroprotection after KCl withdrawal was not observed with 15-deoxy PGJ2. Despite the absence of Neuroprotection, 15-deoxy PGJ2 markedly inhibited the early up-regulation of c-Jun during KCl withdrawal. These studies suggest that ciglitazone and 15-deoxy PGJ2 have markedly different effects on inherent and low-KCl-induced toxicity and c-Jun expression in CGN, indicating potential non-PPAR mechanisms.
N. A. Holman - One of the best experts on this subject based on the ideXlab platform.
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effects of peroxisome proliferator activated receptor γ ligands ciglitazone and 15 deoxy δ12 14 prostaglandin j2 on rat cultured cerebellar granule neuronal viability
Journal of Neuroscience Research, 2003Co-Authors: Steven A Smith, Jodie A Robinson, N. A. Holman, Gregory R. Monteith, Sarah J RobertsthomsonAbstract:Peroxisome proliferator-activated receptor gamma (PPARgamma) has been the focus of studies assessing its potential neuroprotective role. These studies have shown either Neuroprotection or neurotoxicity by PPARgamma ligands. Comparison of these studies is complicated by the use of different PPARgamma ligands, mechanisms of neurotoxicity induction, and neuronal cell type. In this study, we compared the effects of the synthetic PPARgamma ligand ciglitazone with an endogenous PPARgamma ligand, 15-deoxy-delta(12,14)-prostaglandin J(2) (15-deoxy PGJ(2)), on inherent neurotoxicity and Neuroprotection using a reduction in extracellular KCl in rat cultured cerebellar granule neurons (CGN). We also assessed the effects of these ligands on c-Jun protein expression, which is up-regulated on induction of low-KCl-mediated neuronal apoptosis as well as being associated with PPAR in other cell types. We showed that PPARgamma mRNA is expressed in CGN cultures and observed ciglitazone- and 15-deoxy PGJ(2)-mediated inherent neurotoxicity that was concentration and time dependent. c-Jun was only modestly increased in the presence of ciglitazone but was markedly up-regulated by 15-deoxy PGJ(2) after 12 hr. Treatment of CGN cultures with ciglitazone simultaneous with KCl withdrawal resulted in a modest, time-dependent Neuroprotection. Such Neuroprotection after KCl withdrawal was not observed with 15-deoxy PGJ(2). Despite the absence of Neuroprotection, 15-deoxy PGJ(2) markedly inhibited the early up-regulation of c-Jun during KCl withdrawal. These studies suggest that ciglitazone and 15-deoxy PGJ(2) have markedly different effects on inherent and low-KCl-induced toxicity and c-Jun expression in CGN, indicating potential non-PPARgamma mechanisms.
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effects of peroxisome proliferator activated receptor gamma ligands ciglitazone and 15 deoxy delta 12 14 prostaglandin j2 on rat cultured cerebellar granule neuronal viability steven a smith gregory r monteith nicola a holman jodie a robinson fiona j
Journal of Neuroscience Research, 2003Co-Authors: Steven A Smith, Jodie A Robinson, N. A. Holman, Gregory R. Monteith, Sarah J RobertsthomsonAbstract:Peroxisome proliferator-activated receptor (PPAR) has been the focus of studies assessing its potential neuroprotective role. These studies have shown either Neuroprotection or neurotoxicity by PPAR ligands. Comparison of these studies is complicated by the use of different PPAR ligands, mechanisms of neurotoxicity induction, and neuronal cell type. In this study, we compared the effects of the synthetic PPAR ligand ciglitazone with an endogenous PPAR ligand, 15-deoxy-12,14-prostaglandin J2 (15-deoxy PGJ2), on inherent neurotoxicity and Neuroprotection using a reduction in extracellular KCl in rat cultured cerebellar granule neurons (CGN). We also assessed the effects of these ligands on c-Jun protein expression, which is up-regulated on induction of low-KCl-mediated neuronal apoptosis as well as being associated with PPAR in other cell types. We showed that PPAR mRNA is expressed in CGN cultures and observed ciglitazone- and 15-deoxy PGJ2-mediated inherent neurotoxicity that was concentration and time dependent. c-Jun was only modestly increased in the presence of ciglitazone but was markedly up-regulated by 15-deoxy PGJ2 after 12 hr. Treatment of CGN cultures with ciglitazone simultaneous with KCl withdrawal resulted in a modest, time-dependent Neuroprotection. Such Neuroprotection after KCl withdrawal was not observed with 15-deoxy PGJ2. Despite the absence of Neuroprotection, 15-deoxy PGJ2 markedly inhibited the early up-regulation of c-Jun during KCl withdrawal. These studies suggest that ciglitazone and 15-deoxy PGJ2 have markedly different effects on inherent and low-KCl-induced toxicity and c-Jun expression in CGN, indicating potential non-PPAR mechanisms.
Gregory R. Monteith - One of the best experts on this subject based on the ideXlab platform.
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effects of peroxisome proliferator activated receptor γ ligands ciglitazone and 15 deoxy δ12 14 prostaglandin j2 on rat cultured cerebellar granule neuronal viability
Journal of Neuroscience Research, 2003Co-Authors: Steven A Smith, Jodie A Robinson, N. A. Holman, Gregory R. Monteith, Sarah J RobertsthomsonAbstract:Peroxisome proliferator-activated receptor gamma (PPARgamma) has been the focus of studies assessing its potential neuroprotective role. These studies have shown either Neuroprotection or neurotoxicity by PPARgamma ligands. Comparison of these studies is complicated by the use of different PPARgamma ligands, mechanisms of neurotoxicity induction, and neuronal cell type. In this study, we compared the effects of the synthetic PPARgamma ligand ciglitazone with an endogenous PPARgamma ligand, 15-deoxy-delta(12,14)-prostaglandin J(2) (15-deoxy PGJ(2)), on inherent neurotoxicity and Neuroprotection using a reduction in extracellular KCl in rat cultured cerebellar granule neurons (CGN). We also assessed the effects of these ligands on c-Jun protein expression, which is up-regulated on induction of low-KCl-mediated neuronal apoptosis as well as being associated with PPAR in other cell types. We showed that PPARgamma mRNA is expressed in CGN cultures and observed ciglitazone- and 15-deoxy PGJ(2)-mediated inherent neurotoxicity that was concentration and time dependent. c-Jun was only modestly increased in the presence of ciglitazone but was markedly up-regulated by 15-deoxy PGJ(2) after 12 hr. Treatment of CGN cultures with ciglitazone simultaneous with KCl withdrawal resulted in a modest, time-dependent Neuroprotection. Such Neuroprotection after KCl withdrawal was not observed with 15-deoxy PGJ(2). Despite the absence of Neuroprotection, 15-deoxy PGJ(2) markedly inhibited the early up-regulation of c-Jun during KCl withdrawal. These studies suggest that ciglitazone and 15-deoxy PGJ(2) have markedly different effects on inherent and low-KCl-induced toxicity and c-Jun expression in CGN, indicating potential non-PPARgamma mechanisms.
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effects of peroxisome proliferator activated receptor gamma ligands ciglitazone and 15 deoxy delta 12 14 prostaglandin j2 on rat cultured cerebellar granule neuronal viability steven a smith gregory r monteith nicola a holman jodie a robinson fiona j
Journal of Neuroscience Research, 2003Co-Authors: Steven A Smith, Jodie A Robinson, N. A. Holman, Gregory R. Monteith, Sarah J RobertsthomsonAbstract:Peroxisome proliferator-activated receptor (PPAR) has been the focus of studies assessing its potential neuroprotective role. These studies have shown either Neuroprotection or neurotoxicity by PPAR ligands. Comparison of these studies is complicated by the use of different PPAR ligands, mechanisms of neurotoxicity induction, and neuronal cell type. In this study, we compared the effects of the synthetic PPAR ligand ciglitazone with an endogenous PPAR ligand, 15-deoxy-12,14-prostaglandin J2 (15-deoxy PGJ2), on inherent neurotoxicity and Neuroprotection using a reduction in extracellular KCl in rat cultured cerebellar granule neurons (CGN). We also assessed the effects of these ligands on c-Jun protein expression, which is up-regulated on induction of low-KCl-mediated neuronal apoptosis as well as being associated with PPAR in other cell types. We showed that PPAR mRNA is expressed in CGN cultures and observed ciglitazone- and 15-deoxy PGJ2-mediated inherent neurotoxicity that was concentration and time dependent. c-Jun was only modestly increased in the presence of ciglitazone but was markedly up-regulated by 15-deoxy PGJ2 after 12 hr. Treatment of CGN cultures with ciglitazone simultaneous with KCl withdrawal resulted in a modest, time-dependent Neuroprotection. Such Neuroprotection after KCl withdrawal was not observed with 15-deoxy PGJ2. Despite the absence of Neuroprotection, 15-deoxy PGJ2 markedly inhibited the early up-regulation of c-Jun during KCl withdrawal. These studies suggest that ciglitazone and 15-deoxy PGJ2 have markedly different effects on inherent and low-KCl-induced toxicity and c-Jun expression in CGN, indicating potential non-PPAR mechanisms.
