Ferreira 2017 MITOEAGLE Obergurgl

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Ferreira Luciana
Doxorubicin toxicity and mitochondrial dysfunction in mouse induced pluripotent stem cells-derived cardiomyocytes.

Link: MitoEAGLE

Cunha-Oliveira T, Ferreira LL, Coelho AR, Deus CM, Oliveira PJ (2017)

Event: MitoEAGLE Obergurgl 2017

COST Action MitoEAGLE

Doxorubicin (DOX) is a widely used anticancer drug with a limited clinical use because of dose-dependent and cumulative cardiotoxicity. The research on valid strategies to avoid DOX cardiotoxicity involves investigating the mechanisms of toxicity in reliable biological models. DOX-induced cardiotoxicity has been studied in different in vitro models although only a few represent a true cardiac cell model, with the ability to beat in culture.

In this work we used cultured mouse induced pluripotent stem cells (iPSC)-derived cardiomyocytes treated with 0.5 and 1 µM DOX, and measured morphological, functional and biochemical alterations associated with mitochondrial bioenergetics, cellular metabolism, DNA-damage stress responses and apoptosis.

DOX mostly decreased proteins and transcripts associated with mitochondrial bioenergetics and induced p53-dependent caspase activation. Moreover, DOX affected the expression of p53 target transcripts associated with mitochondrial-dependent apoptosis and DNA-damage responses, interestingly in a concentration-independent manner.

In summary, cultured iPSC-derived mouse cardiomyocytes recapitulate markers of DOX cardiotoxicity found in other cardiac-like cell models but also presents some important differences that may be due to the lack of cellular proliferation and/or to the presence of a functional contractile machinery.


Bioblast editor: Kandolf G


Labels: MiParea: Respiration, Pharmacology;toxicology 


Organism: Mouse  Tissue;cell: Heart, Stem cells 




Event: A1, Oral 



Participated at


Affiliations and support

CNC, Center Neuroscience Cell Biol, Univ Coimbra, UC Biotech Building, Biocant Park, Cantanhede, Portugal. - luciana.cl.ferreira@gmail.com


This work was funded by FEDER funds through the Operational Program for Competitiveness Factors—COMPETE and national funds by FCT—Foundation for Science and Technology (PTDC/DTP-FTO/2433/2014 and POCI-01-0145-FEDER-007440). TC-O was supported by a FCT Post-Doctoral fellowship (SFRH/BPD/101169/2014) and LLF (SFRH/BD/52429/2013), ARC (SFRH/BD/103399/2014) and CMD (SFRH/BD/100341/2014) were supported by FCT PhD-fellowships.