Premium
Cyclophilin‐D is dispensable for atrophy and mitochondrial apoptotic signalling in denervated muscle
Author(s) -
Daussin Frederic N.,
Godin Richard,
Ascah Alexis,
Deschênes Sonia,
Burelle Yan
Publication year - 2011
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2010.202036
Subject(s) - denervation , skeletal muscle , mitochondrion , muscle atrophy , microbiology and biotechnology , biology , myocyte , atrophy , mitochondrial permeability transition pore , apoptosis , medicine , endocrinology , biochemistry , programmed cell death
Non‐technical summary Activation of apoptotic cell death signalling by mitochondria is involved in mediating skeletal muscle atrophy following denervation. However, the underlying molecular mechanisms remain unclear, in particular the role of the permeability transition pore (PTP), a high conductance non specific channel of the mitochondrial inner membrane involved in cell death. Using Ppif −/− mice, which are devoid of the PTP sensitizing protein cyclophilin‐D and thus more resistant to pore opening, we directly tested the hypothesis that this pore is involved in atrophy and activation of apoptotic proteolytic signalling following denervation. Our results demonstrate that cyclophilin‐D, and by extension opening of the PTP, is dispensable for atrophy and activation of apoptotic proteolytic signalling induced by denervation.