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Plos One : Inhibition of Doxorubicin-induced Senescence by Pparδ Activation Agonists in Cardiac Muscle Cells ; Cooperation Between Pparδ and Bcl6, Volume 7

By Pintus, Gianfranco

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Book Id: WPLBN0003939567
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Reproduction Date: 2015

Title: Plos One : Inhibition of Doxorubicin-induced Senescence by Pparδ Activation Agonists in Cardiac Muscle Cells ; Cooperation Between Pparδ and Bcl6, Volume 7  
Author: Pintus, Gianfranco
Volume: Volume 7
Language: English
Subject: Journals, Science, Medical Science
Collections: Periodicals: Journal and Magazine Collection (Contemporary)
Historic
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Publisher: Plos

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Pintus, G. (n.d.). Plos One : Inhibition of Doxorubicin-induced Senescence by Pparδ Activation Agonists in Cardiac Muscle Cells ; Cooperation Between Pparδ and Bcl6, Volume 7. Retrieved from http://netlibrary.net/


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Description : Senescence and apoptosis are two distinct cellular programs that are activated in response to a variety of stresses. Low or high doses of the same stressor, i.e., the anticancer drug doxorubicin, may either induce apoptosis or senescence, respectively, in cardiac muscle cells. We have demonstrated that PPARd, a ligand-activated transcriptional factor that controls lipid metabolism, insulin sensitivity and inflammation, is also involved in the doxorubicin-induced senescence program. This occurs through its interference with the transcriptional repressor protein B cell lymphoma-6 (Bcl6). Low doses of doxorubicin increase the expression of PPARd that sequesters Bcl6, thus preventing it from exerting its anti-senescent effects. We also found that L-165041, a specific PPARd activator, is highly effective in protecting cardiomyocytes from doxorubicin-induced senescence through a Bcl6 related mechanism. In fact, L-165041 increases Bcl6 expression via p38, JNK and Akt activation, and at the same time it induces the release of Bcl6 from PPARd, thereby enabling Bcl6 to bind to its target genes. L-165041 also prevented apoptosis induced by higher doses of doxorubicin. However, while experiments performed with siRNA analysis techniques very clearly showed the weight of Bcl6 in the cellular senescence program, no role was found for Bcl6 in the anti-apoptotic effects of L-165041, thus confirming that senescence and apoptosis are two very distinct stress response cellular programs. This study increases our understanding of the molecular mechanism of anthracycline cardiotoxicity and suggests a potential role for PPARd agonists as cardioprotective agents

 

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