Picard 2012 PLoS One: Difference between revisions

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{{Publication
{{Publication
|title=Picard M, Wright KJ, Ritchie D, Thomas MM, Hepple RT (2012) Mitochondrial function in permeabilized cardiomyocytes is largely preserved in the senescent rat myocardium. PLoS One 7: e43003.
|title=Picard M, Wright KJ, Ritchie D, Thomas MM, Hepple RT (2012) Mitochondrial function in permeabilized cardiomyocytes is largely preserved in the senescent rat myocardium. PLoS One 7:e43003.
|info=[http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0043003 PMID: 22912774 Open Access]
|info=[http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0043003 PMID: 22912774 Open Access]
|authors=Picard M, Wright KJ, Ritchie D, Thomas MM, Hepple RT
|authors=Picard M, Wright KJ, Ritchie D, Thomas MM, Hepple RT
Line 13: Line 13:
|tissues=Heart
|tissues=Heart
|preparations=Permeabilized tissue
|preparations=Permeabilized tissue
|enzymes=Complex IV; Cytochrome c Oxidase
|enzymes=Complex IV;cytochrome c oxidase
|injuries=RONS; Oxidative Stress
|injuries=Oxidative stress;RONS
|diseases=Aging; senescence
|diseases=Aging;senescence
|couplingstates=LEAK, OXPHOS
|couplingstates=LEAK, OXPHOS
|substratestates=CI, CIV, CI+II
|pathways=N, CIV, NS
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k
}}
}}

Latest revision as of 09:47, 8 November 2016

Publications in the MiPMap
Has title::Picard M, Wright KJ, Ritchie D, Thomas MM, Hepple RT (2012) Mitochondrial function in permeabilized cardiomyocytes is largely preserved in the senescent rat myocardium. PLoS One 7:e43003.

ยป [[Has info::PMID: 22912774 Open Access]]

Was written by::Picard M, Was written by::Wright KJ, Was written by::Ritchie D, Was written by::Thomas MM, Was written by::Hepple RT (Was published in year::2012) Was published in journal::PLoS One

Abstract: [[has abstract::The aging heart is characterized by a progressive decline in contractile function and diastolic relaxation. Amongst the factors implicated in these changes is a progressive replacement fibrosis secondary to cardiomyoctye death, oxidative damage, and energetic deficit, each of which may be secondary to impaired mitochondrial function. Here, we performed an in-depth examination of mitochondrial function in saponin-permeabilized cardiomyocyte bundles, a preparation where all mitochondria are represented and their structure intact, from young adult (YA) and senescent (SEN) rats (nโ€Š=โ€Š8 per group). When accounting for increased fibrosis (+19%, P<0.01) and proportional decrease in citrate synthase activity in the SEN myocardium (-23%, P<0.05), mitochondrial respiration and reactive oxygen species H2O2 emission across a range of energized states was similar between age groups. Accordingly, the abundance of electron transport chain proteins was also unchanged. Likewise, except for CuZnSOD (-37%, P<0.05), the activity of antioxidant enzymes was unaltered with aging. Although time to mitochondrial permeability transition pore (mPTP) opening was decreased (-25%, P<0.05) in the SEN heart, suggesting sensitization to apoptotic stimuli, this was not associated with a difference in apoptotic index measured by ELISA. Collectively, our results suggest that the function of existing cardiac ventricular mitochondria is relatively preserved in SEN rat heart when measured in permeabilized cells.]] โ€ข Keywords: has publicationkeywords::aging heart, has publicationkeywords::fibrosis, has publicationkeywords::cardiomyoctye death

โ€ข O2k-Network Lab: Was published by MiPNetLab::CA Montreal Hepple RT


Labels: Pathology: Diseases::Aging;senescence  Stress:Injury and adaptation::Oxidative stress;RONS  Organism: Organism::Rat  Tissue;cell: tissue and cell::Heart  Preparation: Preparation::Permeabilized tissue  Enzyme: Enzyme::Complex IV;cytochrome c oxidase 

Coupling state: Coupling states::LEAK, Coupling states::OXPHOS  Pathway: Pathways::N, Pathways::CIV, Pathways::NS  HRR: Instrument and method::Oxygraph-2k 


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