author_facet Patzer, Andreas
Zhao, Yi
Stöck, Ivonne
Gohlke, Peter
Herdegen, Thomas
Culman, Juraj
Patzer, Andreas
Zhao, Yi
Stöck, Ivonne
Gohlke, Peter
Herdegen, Thomas
Culman, Juraj
author Patzer, Andreas
Zhao, Yi
Stöck, Ivonne
Gohlke, Peter
Herdegen, Thomas
Culman, Juraj
spellingShingle Patzer, Andreas
Zhao, Yi
Stöck, Ivonne
Gohlke, Peter
Herdegen, Thomas
Culman, Juraj
European Journal of Neuroscience
Peroxisome proliferator‐activated receptorsγ (PPARγ) differently modulate the interleukin‐6 expression in the peri‐infarct cortical tissue in the acute and delayed phases of cerebral ischaemia
General Neuroscience
author_sort patzer, andreas
spelling Patzer, Andreas Zhao, Yi Stöck, Ivonne Gohlke, Peter Herdegen, Thomas Culman, Juraj 0953-816X 1460-9568 Wiley General Neuroscience http://dx.doi.org/10.1111/j.1460-9568.2008.06478.x <jats:title>Abstract</jats:title><jats:p>Interleukin‐6 (IL‐6) exerts neuroprotective effects after cerebral ischaemia but can also exacerbate inflammation and induce neuronal death. The current study investigates the role of cerebral peroxisome proliferator‐activated receptor(s) γ (PPARγ) in the regulation of IL‐6 expression in the peri‐infarct cortical tissue in rats exposed to focal cerebral ischaemia. Pioglitazone, a high‐affinity PPARγ ligand, was infused intracerebroventricularly (i.c.v.) via osmotic minipumps over a 5‐day period before, during and 24 h or 48 h after middle cerebral artery occlusion (MCAO) for 90 min followed by reperfusion. The expression of PPARγ and IL‐6 in cortical tissue adjacent to the ischaemic core was studied 24 h and 48 h after MCAO. Pioglitazone augmented the ischaemia‐induced upregulation of PPARγ at both time points. Cerebral ischaemia substantially increased IL‐6 expression in the peri‐infarct cortical tissue. Twenty‐four hours after MCAO, the majority of microglial cells/macrophages showed an intense IL‐6 immunoreactivity. IL‐6 was also localized in neurons, but the distribution of neurons positively stained for IL‐6 at the border of the infarct was very heterogeneous. Pioglitazone effectively decreased the number of IL‐6‐immunoreactive cells and IL‐6 protein levels at 24 h but not at 48 h after MCAO. Pioglitazone treatment reduced the infarct size and improved neurological functions. The present study demonstrates that cerebral PPARγ suppresses the expression of IL‐6 in ischaemic brain tissue during the initial phase of ischaemic stroke, in which the overproduction of IL‐6 may aggravate neuronal damage, but not at later time points, when IL‐6 promotes neuroprotection and inhibits neuronal death.</jats:p> Peroxisome proliferator‐activated receptorsγ (PPARγ) differently modulate the interleukin‐6 expression in the peri‐infarct cortical tissue in the acute and delayed phases of cerebral ischaemia European Journal of Neuroscience
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title Peroxisome proliferator‐activated receptorsγ (PPARγ) differently modulate the interleukin‐6 expression in the peri‐infarct cortical tissue in the acute and delayed phases of cerebral ischaemia
title_unstemmed Peroxisome proliferator‐activated receptorsγ (PPARγ) differently modulate the interleukin‐6 expression in the peri‐infarct cortical tissue in the acute and delayed phases of cerebral ischaemia
title_full Peroxisome proliferator‐activated receptorsγ (PPARγ) differently modulate the interleukin‐6 expression in the peri‐infarct cortical tissue in the acute and delayed phases of cerebral ischaemia
title_fullStr Peroxisome proliferator‐activated receptorsγ (PPARγ) differently modulate the interleukin‐6 expression in the peri‐infarct cortical tissue in the acute and delayed phases of cerebral ischaemia
title_full_unstemmed Peroxisome proliferator‐activated receptorsγ (PPARγ) differently modulate the interleukin‐6 expression in the peri‐infarct cortical tissue in the acute and delayed phases of cerebral ischaemia
title_short Peroxisome proliferator‐activated receptorsγ (PPARγ) differently modulate the interleukin‐6 expression in the peri‐infarct cortical tissue in the acute and delayed phases of cerebral ischaemia
title_sort peroxisome proliferator‐activated receptorsγ (pparγ) differently modulate the interleukin‐6 expression in the peri‐infarct cortical tissue in the acute and delayed phases of cerebral ischaemia
topic General Neuroscience
url http://dx.doi.org/10.1111/j.1460-9568.2008.06478.x
publishDate 2008
physical 1786-1794
description <jats:title>Abstract</jats:title><jats:p>Interleukin‐6 (IL‐6) exerts neuroprotective effects after cerebral ischaemia but can also exacerbate inflammation and induce neuronal death. The current study investigates the role of cerebral peroxisome proliferator‐activated receptor(s) γ (PPARγ) in the regulation of IL‐6 expression in the peri‐infarct cortical tissue in rats exposed to focal cerebral ischaemia. Pioglitazone, a high‐affinity PPARγ ligand, was infused intracerebroventricularly (i.c.v.) via osmotic minipumps over a 5‐day period before, during and 24 h or 48 h after middle cerebral artery occlusion (MCAO) for 90 min followed by reperfusion. The expression of PPARγ and IL‐6 in cortical tissue adjacent to the ischaemic core was studied 24 h and 48 h after MCAO. Pioglitazone augmented the ischaemia‐induced upregulation of PPARγ at both time points. Cerebral ischaemia substantially increased IL‐6 expression in the peri‐infarct cortical tissue. Twenty‐four hours after MCAO, the majority of microglial cells/macrophages showed an intense IL‐6 immunoreactivity. IL‐6 was also localized in neurons, but the distribution of neurons positively stained for IL‐6 at the border of the infarct was very heterogeneous. Pioglitazone effectively decreased the number of IL‐6‐immunoreactive cells and IL‐6 protein levels at 24 h but not at 48 h after MCAO. Pioglitazone treatment reduced the infarct size and improved neurological functions. The present study demonstrates that cerebral PPARγ suppresses the expression of IL‐6 in ischaemic brain tissue during the initial phase of ischaemic stroke, in which the overproduction of IL‐6 may aggravate neuronal damage, but not at later time points, when IL‐6 promotes neuroprotection and inhibits neuronal death.</jats:p>
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author Patzer, Andreas, Zhao, Yi, Stöck, Ivonne, Gohlke, Peter, Herdegen, Thomas, Culman, Juraj
author_facet Patzer, Andreas, Zhao, Yi, Stöck, Ivonne, Gohlke, Peter, Herdegen, Thomas, Culman, Juraj, Patzer, Andreas, Zhao, Yi, Stöck, Ivonne, Gohlke, Peter, Herdegen, Thomas, Culman, Juraj
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description <jats:title>Abstract</jats:title><jats:p>Interleukin‐6 (IL‐6) exerts neuroprotective effects after cerebral ischaemia but can also exacerbate inflammation and induce neuronal death. The current study investigates the role of cerebral peroxisome proliferator‐activated receptor(s) γ (PPARγ) in the regulation of IL‐6 expression in the peri‐infarct cortical tissue in rats exposed to focal cerebral ischaemia. Pioglitazone, a high‐affinity PPARγ ligand, was infused intracerebroventricularly (i.c.v.) via osmotic minipumps over a 5‐day period before, during and 24 h or 48 h after middle cerebral artery occlusion (MCAO) for 90 min followed by reperfusion. The expression of PPARγ and IL‐6 in cortical tissue adjacent to the ischaemic core was studied 24 h and 48 h after MCAO. Pioglitazone augmented the ischaemia‐induced upregulation of PPARγ at both time points. Cerebral ischaemia substantially increased IL‐6 expression in the peri‐infarct cortical tissue. Twenty‐four hours after MCAO, the majority of microglial cells/macrophages showed an intense IL‐6 immunoreactivity. IL‐6 was also localized in neurons, but the distribution of neurons positively stained for IL‐6 at the border of the infarct was very heterogeneous. Pioglitazone effectively decreased the number of IL‐6‐immunoreactive cells and IL‐6 protein levels at 24 h but not at 48 h after MCAO. Pioglitazone treatment reduced the infarct size and improved neurological functions. The present study demonstrates that cerebral PPARγ suppresses the expression of IL‐6 in ischaemic brain tissue during the initial phase of ischaemic stroke, in which the overproduction of IL‐6 may aggravate neuronal damage, but not at later time points, when IL‐6 promotes neuroprotection and inhibits neuronal death.</jats:p>
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spelling Patzer, Andreas Zhao, Yi Stöck, Ivonne Gohlke, Peter Herdegen, Thomas Culman, Juraj 0953-816X 1460-9568 Wiley General Neuroscience http://dx.doi.org/10.1111/j.1460-9568.2008.06478.x <jats:title>Abstract</jats:title><jats:p>Interleukin‐6 (IL‐6) exerts neuroprotective effects after cerebral ischaemia but can also exacerbate inflammation and induce neuronal death. The current study investigates the role of cerebral peroxisome proliferator‐activated receptor(s) γ (PPARγ) in the regulation of IL‐6 expression in the peri‐infarct cortical tissue in rats exposed to focal cerebral ischaemia. Pioglitazone, a high‐affinity PPARγ ligand, was infused intracerebroventricularly (i.c.v.) via osmotic minipumps over a 5‐day period before, during and 24 h or 48 h after middle cerebral artery occlusion (MCAO) for 90 min followed by reperfusion. The expression of PPARγ and IL‐6 in cortical tissue adjacent to the ischaemic core was studied 24 h and 48 h after MCAO. Pioglitazone augmented the ischaemia‐induced upregulation of PPARγ at both time points. Cerebral ischaemia substantially increased IL‐6 expression in the peri‐infarct cortical tissue. Twenty‐four hours after MCAO, the majority of microglial cells/macrophages showed an intense IL‐6 immunoreactivity. IL‐6 was also localized in neurons, but the distribution of neurons positively stained for IL‐6 at the border of the infarct was very heterogeneous. Pioglitazone effectively decreased the number of IL‐6‐immunoreactive cells and IL‐6 protein levels at 24 h but not at 48 h after MCAO. Pioglitazone treatment reduced the infarct size and improved neurological functions. The present study demonstrates that cerebral PPARγ suppresses the expression of IL‐6 in ischaemic brain tissue during the initial phase of ischaemic stroke, in which the overproduction of IL‐6 may aggravate neuronal damage, but not at later time points, when IL‐6 promotes neuroprotection and inhibits neuronal death.</jats:p> Peroxisome proliferator‐activated receptorsγ (PPARγ) differently modulate the interleukin‐6 expression in the peri‐infarct cortical tissue in the acute and delayed phases of cerebral ischaemia European Journal of Neuroscience
spellingShingle Patzer, Andreas, Zhao, Yi, Stöck, Ivonne, Gohlke, Peter, Herdegen, Thomas, Culman, Juraj, European Journal of Neuroscience, Peroxisome proliferator‐activated receptorsγ (PPARγ) differently modulate the interleukin‐6 expression in the peri‐infarct cortical tissue in the acute and delayed phases of cerebral ischaemia, General Neuroscience
title Peroxisome proliferator‐activated receptorsγ (PPARγ) differently modulate the interleukin‐6 expression in the peri‐infarct cortical tissue in the acute and delayed phases of cerebral ischaemia
title_full Peroxisome proliferator‐activated receptorsγ (PPARγ) differently modulate the interleukin‐6 expression in the peri‐infarct cortical tissue in the acute and delayed phases of cerebral ischaemia
title_fullStr Peroxisome proliferator‐activated receptorsγ (PPARγ) differently modulate the interleukin‐6 expression in the peri‐infarct cortical tissue in the acute and delayed phases of cerebral ischaemia
title_full_unstemmed Peroxisome proliferator‐activated receptorsγ (PPARγ) differently modulate the interleukin‐6 expression in the peri‐infarct cortical tissue in the acute and delayed phases of cerebral ischaemia
title_short Peroxisome proliferator‐activated receptorsγ (PPARγ) differently modulate the interleukin‐6 expression in the peri‐infarct cortical tissue in the acute and delayed phases of cerebral ischaemia
title_sort peroxisome proliferator‐activated receptorsγ (pparγ) differently modulate the interleukin‐6 expression in the peri‐infarct cortical tissue in the acute and delayed phases of cerebral ischaemia
title_unstemmed Peroxisome proliferator‐activated receptorsγ (PPARγ) differently modulate the interleukin‐6 expression in the peri‐infarct cortical tissue in the acute and delayed phases of cerebral ischaemia
topic General Neuroscience
url http://dx.doi.org/10.1111/j.1460-9568.2008.06478.x