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  • 1
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    Endonuclease G is a novel determinant of cardiac hypertrophy and mitochondrial function (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-10-08
    Description: Left ventricular mass (LVM) is a highly heritable trait and an independent risk factor for all-cause mortality. So far, genome-wide association studies have not identified the genetic factors that underlie LVM variation, and the regulatory mechanisms for blood-pressure-independent cardiac hypertrophy remain poorly understood. Unbiased systems genetics approaches in the rat now provide a powerful complementary tool to genome-wide association studies, and we applied integrative genomics to dissect a highly replicated, blood-pressure-independent LVM locus on rat chromosome 3p. Here we identified endonuclease G (Endog), which previously was implicated in apoptosis but not hypertrophy, as the gene at the locus, and we found a loss-of-function mutation in Endog that is associated with increased LVM and impaired cardiac function. Inhibition of Endog in cultured cardiomyocytes resulted in an increase in cell size and hypertrophic biomarkers in the absence of pro-hypertrophic stimulation. Genome-wide network analysis unexpectedly implicated ENDOG in fundamental mitochondrial processes that are unrelated to apoptosis. We showed direct regulation of ENDOG by ERR-alpha and PGC1alpha (which are master regulators of mitochondrial and cardiac function), interaction of ENDOG with the mitochondrial genome and ENDOG-mediated regulation of mitochondrial mass. At baseline, the Endog-deleted mouse heart had depleted mitochondria, mitochondrial dysfunction and elevated levels of reactive oxygen species, which were associated with enlarged and steatotic cardiomyocytes. Our study has further established the link between mitochondrial dysfunction, reactive oxygen species and heart disease and has uncovered a role for Endog in maladaptive cardiac hypertrophy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3189541/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3189541/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDermott-Roe, Chris -- Ye, Junmei -- Ahmed, Rizwan -- Sun, Xi-Ming -- Serafin, Anna -- Ware, James -- Bottolo, Leonardo -- Muckett, Phil -- Canas, Xavier -- Zhang, Jisheng -- Rowe, Glenn C -- Buchan, Rachel -- Lu, Han -- Braithwaite, Adam -- Mancini, Massimiliano -- Hauton, David -- Marti, Ramon -- Garcia-Arumi, Elena -- Hubner, Norbert -- Jacob, Howard -- Serikawa, Tadao -- Zidek, Vaclav -- Papousek, Frantisek -- Kolar, Frantisek -- Cardona, Maria -- Ruiz-Meana, Marisol -- Garcia-Dorado, David -- Comella, Joan X -- Felkin, Leanne E -- Barton, Paul J R -- Arany, Zoltan -- Pravenec, Michal -- Petretto, Enrico -- Sanchis, Daniel -- Cook, Stuart A -- 087183/Wellcome Trust/United Kingdom -- MC_U120085815/Medical Research Council/United Kingdom -- MC_U120097112/Medical Research Council/United Kingdom -- British Heart Foundation/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2011 Oct 5;478(7367):114-8. doi: 10.1038/nature10490.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Hammersmith Hospital, Du Cane Road, London W12 ONN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21979051" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Body Weight/genetics ; Cardiomegaly/*enzymology/genetics/*pathology/physiopathology ; Cell Respiration ; Chromosomes, Mammalian/genetics ; Crosses, Genetic ; Endodeoxyribonucleases/deficiency/genetics/*metabolism ; Female ; Gene Expression Regulation ; Genes, Mitochondrial/genetics ; Hypertrophy, Left Ventricular/enzymology/genetics/pathology/physiopathology ; Lipid Metabolism ; Male ; Mitochondria/genetics/*metabolism/pathology ; Organ Size/genetics ; Quantitative Trait Loci/genetics ; RNA-Binding Proteins/metabolism ; Rats ; Rats, Inbred Strains ; Reactive Oxygen Species/metabolism ; Receptors, Estrogen/metabolism ; Transcription Factors/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Cardiac angiogenic imbalance leads to peripartum cardiomyopathy (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-05-19
    Description: Peripartum cardiomyopathy (PPCM) is an often fatal disease that affects pregnant women who are near delivery, and it occurs more frequently in women with pre-eclampsia and/or multiple gestation. The aetiology of PPCM, and why it is associated with pre-eclampsia, remain unknown. Here we show that PPCM is associated with a systemic angiogenic imbalance, accentuated by pre-eclampsia. Mice that lack cardiac PGC-1alpha, a powerful regulator of angiogenesis, develop profound PPCM. Importantly, the PPCM is entirely rescued by pro-angiogenic therapies. In humans, the placenta in late gestation secretes VEGF inhibitors like soluble FLT1 (sFLT1), and this is accentuated by multiple gestation and pre-eclampsia. This anti-angiogenic environment is accompanied by subclinical cardiac dysfunction, the extent of which correlates with circulating levels of sFLT1. Exogenous sFLT1 alone caused diastolic dysfunction in wild-type mice, and profound systolic dysfunction in mice lacking cardiac PGC-1alpha. Finally, plasma samples from women with PPCM contained abnormally high levels of sFLT1. These data indicate that PPCM is mainly a vascular disease, caused by excess anti-angiogenic signalling in the peripartum period. The data also explain how late pregnancy poses a threat to cardiac homeostasis, and why pre-eclampsia and multiple gestation are important risk factors for the development of PPCM.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3356917/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3356917/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Patten, Ian S -- Rana, Sarosh -- Shahul, Sajid -- Rowe, Glenn C -- Jang, Cholsoon -- Liu, Laura -- Hacker, Michele R -- Rhee, Julie S -- Mitchell, John -- Mahmood, Feroze -- Hess, Philip -- Farrell, Caitlin -- Koulisis, Nicole -- Khankin, Eliyahu V -- Burke, Suzanne D -- Tudorache, Igor -- Bauersachs, Johann -- del Monte, Federica -- Hilfiker-Kleiner, Denise -- Karumanchi, S Ananth -- Arany, Zoltan -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 May 9;485(7398):333-8. doi: 10.1038/nature11040.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiovascular Institute, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22596155" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bromocriptine/pharmacology/therapeutic use ; Cardiomyopathies/blood/drug therapy/*etiology/*physiopathology ; Disease Models, Animal ; Female ; Heart/drug effects/physiopathology ; Humans ; Kaplan-Meier Estimate ; Male ; Mice ; Mice, Knockout ; Myocytes, Cardiac/drug effects/metabolism ; Neovascularization, Pathologic/*complications/drug therapy/*physiopathology ; Neovascularization, Physiologic/drug effects/physiology ; Pre-Eclampsia/physiopathology ; Pregnancy ; Pregnancy Complications, Cardiovascular/blood/drug ; therapy/*etiology/*physiopathology ; Trans-Activators/deficiency/genetics/metabolism ; Transcription Factors ; Vascular Endothelial Growth Factor A/pharmacology/therapeutic use ; Vascular Endothelial Growth Factor ; Receptor-1/blood/genetics/metabolism/pharmacology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    Skeletal muscle transcriptional coactivator PGC-1  mediates mitochondrial, but not metabolic, changes during calorie restriction (2012)
    National Academy of Sciences
    Details
    Publication Date: 2012-02-03
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 4
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    Skeletal muscle transcriptional coactivator PGC-1{alpha} mediates mitochondrial, but not metabolic, changes during calorie restriction [Cell Biology] (2012)
    National Academy of Sciences
    Details
    Publication Date: 2012-02-22
    Description: Calorie restriction (CR) is a dietary intervention that extends lifespan and healthspan in a variety of organisms. CR improves mitochondrial energy production, fuel oxidation, and reactive oxygen species (ROS) scavenging in skeletal muscle and other tissues, and these processes are thought to be critical to the benefits of CR. PGC-1α is a transcriptional coactivator that regulates mitochondrial function and is induced by CR. Consequently, many of the mitochondrial and metabolic benefits of CR are attributed to increased PGC-1α activity. To test this model, we examined the metabolic and mitochondrial response to CR in mice lacking skeletal muscle PGC-1α (MKO). Surprisingly, MKO mice demonstrated a normal improvement in glucose homeostasis in response to CR, indicating that skeletal muscle PGC-1α is dispensable for the whole-body benefits of CR. In contrast, gene expression profiling and electron microscopy (EM) demonstrated that PGC-1α is required for the full CR-induced increases in mitochondrial gene expression and mitochondrial density in skeletal muscle. These results demonstrate that PGC-1α is a major regulator of the mitochondrial response to CR in skeletal muscle, but surprisingly show that neither PGC-1α nor mitochondrial biogenesis in skeletal muscle are required for the whole-body metabolic benefits of CR.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 5
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    Positron lifetime measurements of hydrogen passivation of cation vacancies in yttrium aluminum oxide garnets (2013)
    American Physical Society (APS)
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    Publication Date: 2013-11-05
    Description: Author(s): F. A. Selim, C. R. Varney, M. C. Tarun, M. C. Rowe, G. S. Collins, and M. D. McCluskey A charge compensation mechanism is proposed for cation vacancy defects in complex oxides based on positron lifetime measurements, infrared spectroscopy, and composition analysis. Defects were characterized in samples of yttrium aluminum garnet grown in O 2 or Ar. However, no positron trapping was det... [Phys. Rev. B 88, 174102] Published Mon Nov 04, 2013
    Keywords: Structure, structural phase transitions, mechanical properties, defects
    Print ISSN: 1098-0121
    Electronic ISSN: 1095-3795
    Topics: Physics
    Published by American Physical Society (APS)
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