Lemieux 2012 J Bioenerg Biomembr
| Lemieux H, Warren BE (2012) An animal model to study human muscular diseases involving mitochondrial oxidative phosphorylation. J Bioenerg Biomembr 44:503-12. |
Lemieux H, Warren BE (2012) J Bioenerg Biomembr
Abstract: Mitochondria are producing most of the energy needed for many cellular functions by a process named oxidative phosphorylation (OXPHOS). It is now well recognized that mitochondrial dysfunctions are involved in several pathologies or degenerative processes, including cardiovascular diseases, diabetes, and aging. Animal models are currently used to try to understand the role of mitochondria in human diseases but a major problem is that mitochondria from different species and tissues are variable in terms of regulation. Analysis of mitochondrial function in three species of planarian flatworms (Tricladia, Platyhelminthes) shows that they share a very rare characteristic with human mitochondria: a strong control of oxidative phosphorylation by the phosphorylation system. The ratio of coupled OXPHOS over maximal electron transport capacity after uncoupling (electron transport system; ET-pathway) well below 1.0 indicates that the phosphorylation system is limiting the rate of OXPHOS. The OXPHOS/ET-pathway ratios are 0.62 ± 0.06 in Dugesia tigrina, 0.63 ± 0.05 in D. dorotocephala and 0.62 ± 0.05 in Procotyla fluviatilis, comparable to the value measured in human muscles. To our knowledge, no other animal model displays this peculiarity. This new model offers a venue in which to test the phosphorylation system as a potential therapeutic control point within humans. • Keywords: Animal model, Cardiovascular disease, Human muscular disease, Planarian phosphorylation system
• O2k-Network Lab: CA Edmonton Lemieux H
Labels: MiParea: Respiration, Comparative MiP;environmental MiP
Organism: Other invertebrates
Preparation: Permeabilized tissue
Coupling state: LEAK, OXPHOS, ET
HRR: Oxygraph-2k
