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Peroxisome-proliferator-activated receptor-gamma (PPARγ) activation protects neurons from NMDA excitotoxicity

Zhao, Xiurong ; Ou, Zhishuo ; Grotta, James C. ; Waxham, Neal ; Aronowski, Jaroslaw

Brain research, 2006-02, Vol.1073, p.460-469 [Periódico revisado por pares]

Netherlands: Elsevier B.V

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Título:
Peroxisome-proliferator-activated receptor-gamma (PPARγ) activation protects neurons from NMDA excitotoxicity
Autor: Zhao, Xiurong ; Ou, Zhishuo ; Grotta, James C. ; Waxham, Neal ; Aronowski, Jaroslaw
Assuntos: 15deoxy-Δ 12,14-Prostaglandin J 2 (15d-PGJ 2) ; Analysis of Variance ; Animals ; Antibodies - pharmacology ; Calcium - metabolism ; Cell Survival - drug effects ; Cells, Cultured ; Cerebral Cortex - pathology ; Ciglitazone ; Diagnostic Imaging - methods ; Dizocilpine Maleate - pharmacology ; Drug Interactions ; Electrophoretic Mobility Shift Assay - methods ; Embryo, Mammalian ; Enzyme Inhibitors - pharmacology ; Excitatory Amino Acid Agonists - toxicity ; Excitatory Amino Acid Antagonists - pharmacology ; Excitotoxicity ; Glutamic Acid - pharmacology ; Hydro-Lyases - metabolism ; Immunohistochemistry - methods ; Male ; Microtubule-Associated Proteins - metabolism ; N-Methylaspartate - toxicity ; Neurons - drug effects ; Neurons - physiology ; Neurons in culture ; Neuroprotection ; Neuroprotective Agents - pharmacology ; PPAR gamma - agonists ; PPAR gamma - antagonists & inhibitors ; PPAR gamma - immunology ; PPAR gamma - pharmacology ; PPARγ ; Propidium ; Rats ; Rats, Sprague-Dawley
É parte de: Brain research, 2006-02, Vol.1073, p.460-469
Notas: ObjectType-Article-1
SourceType-Scholarly Journals-1
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Descrição: A growing body of evidence indicates that the transcription factor PPARγ plays a beneficial role in various neurological diseases. The postulated principal mechanism underlying the beneficial effects of PPARγ is due to its anti-inflammatory properties. However, PPARγ exists in neurons where it may provide additional effects that regulate neuronal vulnerability. In the present study, we employed in vitro and in vivo models of excitotoxic neuronal injury to test hypothesis on the neuroprotective role of PPARγ. The endogenous PPARγ ligand, 15d-Δ 12,14-Prostaglandin J 2 (15d-PGJ 2), and a selective thiazolidinedione PPARγ agonist, ciglitazone, significantly reduced neuronal death in response to glutamate and NMDA-mediated, but not kainate-mediated toxicity. This neuroprotective effect of 15d-PGJ 2 and ciglitazone was linked to increased PPARγ DNA binding activity as it was fully reversed by the pretreatment of neurons with selective PPARγ antagonists and anti-PPARγ antibody. It was not due to the blockade of NMDA-receptor-mediated Ca ++ entry. Our data demonstrate that PPARγ activation may represent a potential target for treatment of numerous acute and chronic neurological diseases with pathologies that involve excitotoxic damage.
Editor: Netherlands: Elsevier B.V
Idioma: Inglês

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Peroxisome-proliferator-activated receptor-gamma (PPARγ) activation protects neurons from NMDA excitotoxicity

Zhao, Xiurong ; Ou, Zhishuo ; Grotta, James C. ; Waxham, Neal ; Aronowski, Jaroslaw

Netherlands: Elsevier B.V

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