Ferreira 2017 MITOEAGLE Obergurgl: Difference between revisions
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{{Abstract | {{Abstract | ||
|title=[[File: | |title=[[File:LFerreira.jpg|left|90px|Ferreira Luciana]] Doxorubicin toxicity and mitochondrial dysfunction in mouse induced pluripotent stem cells-derived cardiomyocytes. | ||
|info=[[ | |info=[[MitoEAGLE]] | ||
|authors=Cunha-Oliveira T, Ferreira LL, Coelho AR, Deus CM, Oliveira PJ | |authors=Cunha-Oliveira T, Ferreira LL, Coelho AR, Deus CM, Oliveira PJ | ||
|year=2017 | |year=2017 | ||
|event= | |event=MitoEAGLE Obergurgl 2017 | ||
|abstract=[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action | |abstract=[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|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.Β | |||
Β | |||
In this work we used cultured mouse induced pluripotent stem cells (iPSC)-derived cardiomyocytes treated with 0.5 and 1 Β΅M DOX, and measured morphological, functional and biochemical alterations associated with mitochondrial bioenergetics, cellular metabolism, DNA-damage stress responses and apoptosis. | |||
Β | |||
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. | |||
Β | |||
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. | |||
|editor=[[Kandolf G]], | |editor=[[Kandolf G]], | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=Pharmacology;toxicology | |area=Respiration, Pharmacology;toxicology | ||
|organism=Mouse | |organism=Mouse | ||
|tissues=Heart, Stem cells | |tissues=Heart, Stem cells | ||
|event=A1, Oral | |||
}} | }} | ||
==Participated at== | |||
::::* [[MiPschool Obergurgl 2017| MiPschool 2017 Obergurgl AT]] | |||
== Affiliations and support== | == Affiliations and support== | ||
::::CNC, Center Neuroscience Cell Biol, Univ Coimbra, UC Biotech Building, Biocant Park, Cantanhede, Portugal. - [email protected] | ::::CNC, Center Neuroscience Cell Biol, Univ Coimbra, UC Biotech Building, Biocant Park, Cantanhede, Portugal. - [email protected] | ||
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::::This work was funded by FEDER funds through the Operational Program for Competitiveness FactorsβCOMPETE and national funds by FCTβFoundation 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. | ::::This work was funded by FEDER funds through the Operational Program for Competitiveness FactorsβCOMPETE and national funds by FCTβFoundation 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. | ||
Latest revision as of 12:52, 18 February 2019
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
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 Β΅M 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.
β’ 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. - [email protected]
- This work was funded by FEDER funds through the Operational Program for Competitiveness FactorsβCOMPETE and national funds by FCTβFoundation 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.