http://www.cnr.it/ontology/cnr/individuo/prodotto/ID202617
Epigallocatechin-3-gallate prevents oxidative phosphorylation deficit and promotes mitochondrial biogenesis in human cells from subjects with Down's syndrome (Articolo in rivista)
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- Epigallocatechin-3-gallate prevents oxidative phosphorylation deficit and promotes mitochondrial biogenesis in human cells from subjects with Down's syndrome (Articolo in rivista) (literal)
- Anno
- 2013-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1016/j.bbadis.2012.12.011 (literal)
- Alternative label
Daniela Valenti, Domenico De Rasmo, Anna Signorile, Leonardo Rossi, Lidia de Bari, Iris Scala, Barbara Granese, Sergio Papa, Rosa Anna Vacca (2013)
Epigallocatechin-3-gallate prevents oxidative phosphorylation deficit and promotes mitochondrial biogenesis in human cells from subjects with Down's syndrome
in Biochimica et biophysica acta. Molecular basis of disease
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- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Daniela Valenti, Domenico De Rasmo, Anna Signorile, Leonardo Rossi, Lidia de Bari, Iris Scala, Barbara Granese, Sergio Papa, Rosa Anna Vacca (literal)
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- Institute of Biomembranes and Bioenergetics, National Council of Research, Bari, Italy;
Department of Basic Medical Sciences, Neuroscience and Sense Organs, University of Bari, Italy;
Laboratory of Biology and Genetics, Department of Clinical and Experimental Medicine, University of Pisa, Italy;
Department of Pediatrics, Federico II University, Naples, Italy (literal)
- Titolo
- Epigallocatechin-3-gallate prevents oxidative phosphorylation deficit and promotes mitochondrial biogenesis in human cells from subjects with Down's syndrome (literal)
- Abstract
- A critical role for mitochondrial dysfunction has been proposed in the pathogenesis of Down's syndrome (DS), a human multifactorial disorder caused by trisomy of chromosome 21, associated with mental retardation and early neurodegeneration. Previous studies from our group demonstrated in DS cells a decreased capacity of the mitochondrial ATP production system and overproduction of reactive oxygen species (ROS) in mitochondria. In this study we have tested the potential of epigallocatechin-3-gallate (EGCG) - a natural polyphenol component of green tea - to counteract the mitochondrial energy deficit found in DS cells. We found that EGCG, incubated with cultured lymphoblasts and fibroblasts from DS subjects, rescued mitochondrial complex I and ATP synthase catalytic activities, restored oxidative phosphorylation efficiency and counteracted oxidative stress. These effects were associated with EGCG-induced promotion of PKA activity, related to increased cellular levels of cAMP and PKA-dependent phosphorylation of the NDUFS4 subunit of complex I. In addition, EGCG strongly promoted mitochondrial biogenesis in DS cells, as associated with increase in Sirt1-dependent PGC-1? deacetylation, NRF-1 and T-FAM protein levels and mitochondrial DNA content.
In conclusion, this study shows that EGCG is a promoting effector of oxidative phosphorylation and mitochondrial biogenesis in DS cells, acting through modulation of the cAMP/PKA- and sirtuin-dependent pathways. EGCG treatment promises thus to be a therapeutic approach to counteract mitochondrial energy deficit and oxidative stress in DS. (literal)
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