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  • 1
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    MicroRNA-34a regulates cardiac ageing and function (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-02-22
    Description: Ageing is the predominant risk factor for cardiovascular diseases and contributes to a significantly worse outcome in patients with acute myocardial infarction. MicroRNAs (miRNAs) have emerged as crucial regulators of cardiovascular function and some miRNAs have key roles in ageing. We propose that altered expression of miRNAs in the heart during ageing contributes to the age-dependent decline in cardiac function. Here we show that miR-34a is induced in the ageing heart and that in vivo silencing or genetic deletion of miR-34a reduces age-associated cardiomyocyte cell death. Moreover, miR-34a inhibition reduces cell death and fibrosis following acute myocardial infarction and improves recovery of myocardial function. Mechanistically, we identified PNUTS (also known as PPP1R10) as a novel direct miR-34a target, which reduces telomere shortening, DNA damage responses and cardiomyocyte apoptosis, and improves functional recovery after acute myocardial infarction. Together, these results identify age-induced expression of miR-34a and inhibition of its target PNUTS as a key mechanism that regulates cardiac contractile function during ageing and after acute myocardial infarction, by inducing DNA damage responses and telomere attrition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boon, Reinier A -- Iekushi, Kazuma -- Lechner, Stefanie -- Seeger, Timon -- Fischer, Ariane -- Heydt, Susanne -- Kaluza, David -- Treguer, Karine -- Carmona, Guillaume -- Bonauer, Angelika -- Horrevoets, Anton J G -- Didier, Nathalie -- Girmatsion, Zenawit -- Biliczki, Peter -- Ehrlich, Joachim R -- Katus, Hugo A -- Muller, Oliver J -- Potente, Michael -- Zeiher, Andreas M -- Hermeking, Heiko -- Dimmeler, Stefanie -- England -- Nature. 2013 Mar 7;495(7439):107-10. doi: 10.1038/nature11919. Epub 2013 Feb 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Cardiovascular Regeneration, Centre of Molecular Medicine, Goethe University Frankfurt, 60590 Frankfurt, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23426265" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/genetics/pathology/*physiology ; Animals ; Apoptosis ; DNA Damage ; Fibrosis/genetics/pathology ; Gene Deletion ; *Gene Expression Regulation ; Gene Knockout Techniques ; Genetic Therapy ; Heart/*physiology ; Mice ; Mice, Inbred C57BL ; MicroRNAs/*genetics/metabolism ; Myocardial Infarction/genetics/pathology/therapy ; Myocardium/cytology/*metabolism/pathology ; Myocytes, Cardiac/cytology/metabolism/pathology ; Substrate Specificity ; Telomere/genetics/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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    Mediation of c-Myc-induced apoptosis by p53 (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-30
    Description: The cellular proto-oncogene c-myc is involved in cell proliferation and transformation but is also implicated in the induction of programmed cell death (apoptosis). The same characteristics have been described for the tumor suppressor gene p53, the most commonly mutated gene in human cancer. In quiescent mouse fibroblasts expressing wild-type p53 protein, activation of c-Myc was found to induce apoptosis and cell cycle reentry, preceded by stabilization of p53. In contrast, in quiescent p53-null fibroblasts, activation of c-Myc induced cell cycle reentry but not apoptosis. These results suggest that p53 mediates apoptosis as a safeguard mechanism to prevent cell proliferation induced by oncogene activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hermeking, H -- Eick, D -- New York, N.Y. -- Science. 1994 Sep 30;265(5181):2091-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut fur Klinische Molekularbiologie und Tumorgenetik Forschungszentrum fur Umwelt und Gesundheit, GSF, Munchen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8091232" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; *Apoptosis ; Cell Line ; Estradiol/pharmacology ; G1 Phase ; Gene Expression Regulation ; Genes, myc ; Genes, p53 ; Mice ; Proto-Oncogene Proteins c-myc/*metabolism ; Tamoxifen/analogs & derivatives/pharmacology ; Transfection ; Tumor Suppressor Protein p53/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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