Difference between revisions of "Neyroud 2019 J Muscle Res Cell Motil"
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Revision as of 15:31, 10 April 2019
Neyroud D, Nosacka RL, Judge AR, Hepple RT (2019) Colon 26 adenocarcinoma (C26)-induced cancer cachexia impairs skeletal muscle mitochondrial function and content. J Muscle Res Cell Motil [Epub ahead of print]. |
Neyroud D, Nosacka RL, Judge AR, Hepple RT (2019) J Muscle Res Cell Motil
Abstract: The present study aimed to determine the impact of colon 26 adenocarcinoma (C26)-induced cancer cachexia on skeletal muscle mitochondrial respiration and content. Twelve male CD2F1 mice were injected with C26-cells (tumor bearing (TB) group), whereas 12 age-matched mice received PBS vehicle injection (non-tumor bearing (N-TB) group). Mitochondrial respiration was studied in saponin-permeabilized soleus myofibers. TB mice showed lower body weight (~β20%) as well as lower soleus, gastrocnemius-plantaris complex and tibialis anterior masses versus N-TB mice (pβ<β0.05). Soleus maximal state III mitochondrial respiration was 20% lower (10 mM glutamate, 5 mM malate, 5 mM adenosine diphosphate; pβ<β0.05) and acceptor control ratio (state III/state II) was 15% lower in the TB vs. N-TB (pβ<β0.05), with the latter suggesting uncoupling. Lower VDAC protein content suggested reduced mitochondrial content in TB versus N-TB (pβ<β0.05). Skeletal muscle in C26-induced cancer cachexia exhibits reductions in: maximal mitochondrial respiration capacity, mitochondrial coupling and mitochondrial content. β’ Keywords: Mitochondrial content, Mitochondrial coupling, Mitochondrial homeostasis, Mitochondrial respiration, Muscle wasting, Oxidative phosphorylation β’ Bioblast editor: Plangger M β’ O2k-Network Lab: US FL Gainesville Hepple RT
Labels: MiParea: Respiration
Pathology: Cancer
Organism: Mouse Tissue;cell: Skeletal muscle Preparation: Permeabilized cells
Coupling state: OXPHOS
Pathway: N, NS
HRR: Oxygraph-2k
Labels, 2019-04