http://www.cnr.it/ontology/cnr/individuo/prodotto/ID21290
PGC-1alpha down-regulation affects the antioxidant response in Friedreich's ataxia. (Articolo in rivista)
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- Label
- PGC-1alpha down-regulation affects the antioxidant response in Friedreich's ataxia. (Articolo in rivista) (literal)
- Anno
- 2010-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1371/journal.pone.0010025 (literal)
- Alternative label
Marmolino D, Manto M, Acquaviva F, Vergara P, Ravella A, MONTICELLI A, Pandolfo M. (2010)
PGC-1alpha down-regulation affects the antioxidant response in Friedreich's ataxia.
in PloS one
(literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Marmolino D, Manto M, Acquaviva F, Vergara P, Ravella A, MONTICELLI A, Pandolfo M. (literal)
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- SCImago (literal)
- PubMe (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- Gruppo Interdipartimentale di Bioinformatica e Biologia Computazionale, Università di Napoli Federico II, Università di Salerno, Naples, Italy
Dipartimento di Biologia e Patologia Cellulare e Molecolare L. Califano, Università degli Studi di Napoli Federico II, Naples, Italy
Dipartimento di Scienze Fisiche, Università degli Studi di Napoli Federico II, Naples, Italy
Istituto Nazionale di Fisica Nucleare - Sezione di Napoli, Naples, Italy
IEOS Istituto di Endocrinologia ed Oncologia Sperimentale, CNR Napoli, Naples, Italy (literal)
- Titolo
- PGC-1alpha down-regulation affects the antioxidant response in Friedreich's ataxia. (literal)
- Abstract
- BACKGROUND: Cells from individuals with Friedreich's ataxia (FRDA) show reduced activities of antioxidant enzymes and cannot up-regulate their expression when exposed to oxidative stress. This blunted antioxidant response may play a central role in the pathogenesis. We previously reported that Peroxisome Proliferator Activated Receptor Gamma (PPARgamma) Coactivator 1-alpha (PGC-1alpha), a transcriptional master regulator of mitochondrial biogenesis and antioxidant responses, is down-regulated in most cell types from FRDA patients and animal models. METHODOLOGY/PRINCIPAL FINDINGS: We used primary fibroblasts from FRDA patients and the knock in-knock out animal model for the disease (KIKO mouse) to determine basal superoxide dismutase 2 (SOD2) levels and the response to oxidative stress induced by the addition of hydrogen peroxide. We measured the same parameters after pharmacological stimulation of PGC-1alpha. Compared to control cells, PGC-1alpha and SOD2 levels were decreased in FRDA cells and did not change after addition of hydrogen peroxide. PGC-1alpha direct silencing with siRNA in control fibroblasts led to a similar loss of SOD2 response to oxidative stress as observed in FRDA fibroblasts. PGC-1alpha activation with the PPARgamma agonist (Pioglitazone) or with a cAMP-dependent protein kinase (AMPK) agonist (AICAR) restored normal SOD2 induction. Treatment of the KIKO mice with Pioglitazone significantly up-regulates SOD2 in cerebellum and spinal cord. CONCLUSIONS/SIGNIFICANCE: PGC-1alpha down-regulation is likely to contribute to the blunted antioxidant response observed in cells from FRDA patients. This response can be restored by AMPK and PPARgamma agonists, suggesting a potential therapeutic approach for FRDA. (literal)
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