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• W2124482434 abstract "Two unresolved aspects of the role of mitochondria-derived cytochrome c in apoptosis are whether there is a separate pool of cytochrome c within mitochondria that participates in the activation of apoptosis and whether a chemically modified cytochrome c drives apoptosis. These questions were investigated using osteoclasts, because they are rich in mitochondria and because osteoclast apoptosis is critical in bone metabolism regulation. H 2 O 2 production was increased during culture, preceding cytochrome c release; both processes occurred anterior to apoptosis. With the addition of a mitochondrial uncoupler, H 2 O 2 production and apoptosis were blocked, indicating the prominent role of mitochondria-derived H 2 O 2 . Trapping H 2 O 2 -derived hydroxyl radical decreased apoptosis. Cytosolic cytochrome c was originated from a single mitochondrial compartment, supporting a common pool involved in respiration and apoptosis, and it was chemically identical to the native form, with no indication of oxidative or nitrative modifications. Protein levels of Bcl-2 and Bc-xL were decreased before apoptosis, whereas expression of wild-type Bcl-2 repressed apoptosis, confirming that cytochrome c release is critical in initiating apoptosis. Cytosolic cytochrome c participated in activating caspase-3 and -9, both required for apoptosis. Collectively, our data indicate that the mitochondria-dependent apoptotic pathway is one of the major routes operating in osteoclasts." @default.
• W2124482434 created "2016-06-24" @default.
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• W2124482434 date "2005-01-01" @default.
• W2124482434 modified "2023-09-23" @default.
• W2124482434 title "Native, not nitrated, cytochromecand mitochondria-derived hydrogen peroxide drive osteoclast apoptosis" @default.
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• W2124482434 doi "https://doi.org/10.1152/ajpcell.00092.2004" @default.
• W2124482434 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15342339" @default.
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