Mouse mammary gland involution is associated with cytochrome c release and caspase activation

At weaning, milk producing mammary epithelial cells undergo apoptosis and are removed by phagocytosis. Here, we show that mouse mammary gland involution is associated with mitochondrial cytochrome c release and processing of numerous caspases, including caspase-1, -3, -7, -8 and -9. Induction of cas...

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Main Authors: Marti, Andreas (Author) , Ritter, Philipp M. (Author) , Jäger, Richard (Author) , Lazar, Hedvika (Author) , Baltzer, Anna (Author) , Schenkel, Johannes (Author) , Declercq, Wim (Author) , Vandenabeele, Peter (Author) , Jaggi, Rolf (Author)
Format: Article (Journal)
Language:English
Published: 6 June 2001
In: Mechanisms of development
Year: 2001, Volume: 104, Issue: 1, Pages: 89-98
ISSN:1872-6356
DOI:10.1016/S0925-4773(01)00381-1
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/S0925-4773(01)00381-1
Verlag, lizenzpflichtig, Volltext: https://www.sciencedirect.com/science/article/pii/S0925477301003811
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Author Notes:Andreas Marti, Philipp M. Ritter, Richard Jäger, Hedvika Lazar, Anna Baltzer, Johannes Schenkel, Wim Declercq, Peter Vandenabeele, Rolf Jaggi

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520 |a At weaning, milk producing mammary epithelial cells undergo apoptosis and are removed by phagocytosis. Here, we show that mouse mammary gland involution is associated with mitochondrial cytochrome c release and processing of numerous caspases, including caspase-1, -3, -7, -8 and -9. Induction of caspase-3-like activity paralleled cleavage of poly-(ADP-ribose) polymerase. Dexamethasone inhibited processing of caspase-3, -7 and -8 and apoptosis, but had no effect on caspase-1 accumulation and cytochrome c release. In Bcl-2 transgenic animals, cytochrome c release, caspase activation and apoptosis were impaired. Thus, the pro-apoptotic signaling pathway in mammary epithelial cells during involution involves the release of cytochrome c and activation of caspases. It is inhibited by Bcl-2 at the mitochondrial level and by dexamethasone at a post-mitochondrial level. 
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