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Göteborgs universitets publikationer

Epigallocatechin-3-gallate induces oxidative phosphorylation by activating cytochrome c oxidase in human cultured neurons and astrocytes

Författare och institution:
G. Castellano-Gonzalez (-); Nicolas Pichaud (Institutionen för biologi och miljövetenskap); J. W. O. Ballard (-); A. Bessede (-); H. Marcal (-); G. J. Guillemin (-)
Publicerad i:
Oncotarget, 7 ( 7 ) s. 7426-7440
Artikel, refereegranskad vetenskaplig
Sammanfattning (abstract):
Mitochondrial dysfunction and resulting energy impairment have been identified as features of many neurodegenerative diseases. Whether this energy impairment is the cause of the disease or the consequence of preceding impairment(s) is still under discussion, however a recovery of cellular bioenergetics would plausibly prevent or improve the pathology. In this study, we screened different natural molecules for their ability to increase intracellular adenine triphosphate purine (ATP). Among them, epigallocatechin-3-gallate (EGCG), a polyphenol from green tea, presented the most striking results. We found that it increases ATP production in both human cultured astrocytes and neurons with different kinetic parameters and without toxicity. Specifically, we showed that oxidative phosphorylation in human cultured astrocytes and neurons increased at the level of the routine respiration on the cells pre-treated with the natural molecule. Furthermore, EGCG-induced ATP production was only blocked by sodium azide (NaN3) and oligomycin, inhibitors of cytochrome c oxidase (CcO; complex IV) and ATP synthase (complex V) respectively. These findings suggest that the EGCG modulates CcO activity, as confirmed by its enzymatic activity. CcO is known to be regulated differently in neurons and astrocytes. Accordingly, EGCG treatment is acting differently on the kinetic parameters of the two cell types. To our knowledge, this is the first study showing that EGCG promotes CcO activity in human cultured neurons and astrocytes. Considering that CcO dysfunction has been reported in patients having neurodegenerative diseases such as Alzheimer's disease (AD), we therefore suggest that EGCG could restore mitochondrial function and prevent subsequent loss of synaptic function.
Ämne (baseras på Högskoleverkets indelning av forskningsämnen):
Biologiska vetenskaper
epigallocatechin-3-gallate, ATP, neurodegeneration, cytochrome c oxidase, mitochondria, Gerotarget, high-resolution respirometry, ampk signaling pathway, green tea, quinolinic acid, mitochondrial dysfunction, metabolic-control, protein-kinase, human-cells, egcg, stress, Oncology, Cell Biology
Postens nummer:
Posten skapad:
2016-03-18 15:32

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