Quaking Inhibits Doxorubicin-Mediated Cardiotoxicity Through Regulation of Cardiac Circular RNA Expression

RBPs (RNA-binding proteins) have been described to be expressed and regulated in various organs including the heart. Little is known about the role of RBPs in heart failure induced by the chemotherapy drug doxorubicin and their interaction with circular RNAs. We aimed to identify key RBPs involved i...

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Vydáno v:Circulation research Ročník 122; číslo 2; s. 246
Hlavní autoři: Gupta, Shashi Kumar, Garg, Ankita, Bär, Christian, Chatterjee, Shambhabi, Foinquinos, Ariana, Milting, Hendrik, Streckfuß-Bömeke, Katrin, Fiedler, Jan, Thum, Thomas
Médium: Journal Article
Jazyk:angličtina
Vydáno: United States 19.01.2018
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ISSN:1524-4571, 1524-4571
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Abstract RBPs (RNA-binding proteins) have been described to be expressed and regulated in various organs including the heart. Little is known about the role of RBPs in heart failure induced by the chemotherapy drug doxorubicin and their interaction with circular RNAs. We aimed to identify key RBPs involved in doxorubicin-mediated heart failure and to elucidate their function. Global transcriptome profiling from murine myocardium exposed to doxorubicin identified 5 differentially expressed RBPs. Expression of the RBP QKI (Quaking) in response to doxorubicin was strongly downregulated in rodent cardiomyocytes and human induced pluripotent stem cell-derived cardiomyocytes in vitro and in vivo in mice. Knockdown of in primary cardiomyocytes increased apoptosis and atrophy after treatment with doxorubicin, whereas lentiviral mediated overexpression of inhibited the doxorubicin-induced apoptosis in cardiomyocytes. In vivo, AAV9 (adeno-associated virus serotype 9)-mediated cardiac overexpression of prevented cardiac apoptosis and cardiac atrophy induced by doxorubicin and improved cardiac function. Mechanistically, by lentiviral-based overexpression and CRISPR/Cas9-mediated silencing of , we identified regulated expression of specific circular RNAs derived from (Titin), (Formin homology 2 domain containing 3), and (Striatin, calmodulin-binding protein 3). Moreover, inhibition of -derived circular RNA increased the susceptibility of cardiomyocytes to doxorubicin. We here show that overexpression of strongly attenuates the toxic effect of doxorubicin via regulating a set of circular RNAs. is, thus, an interesting target molecule to combat doxorubicin-induced cardiotoxicity.
AbstractList RBPs (RNA-binding proteins) have been described to be expressed and regulated in various organs including the heart. Little is known about the role of RBPs in heart failure induced by the chemotherapy drug doxorubicin and their interaction with circular RNAs. We aimed to identify key RBPs involved in doxorubicin-mediated heart failure and to elucidate their function. Global transcriptome profiling from murine myocardium exposed to doxorubicin identified 5 differentially expressed RBPs. Expression of the RBP QKI (Quaking) in response to doxorubicin was strongly downregulated in rodent cardiomyocytes and human induced pluripotent stem cell-derived cardiomyocytes in vitro and in vivo in mice. Knockdown of in primary cardiomyocytes increased apoptosis and atrophy after treatment with doxorubicin, whereas lentiviral mediated overexpression of inhibited the doxorubicin-induced apoptosis in cardiomyocytes. In vivo, AAV9 (adeno-associated virus serotype 9)-mediated cardiac overexpression of prevented cardiac apoptosis and cardiac atrophy induced by doxorubicin and improved cardiac function. Mechanistically, by lentiviral-based overexpression and CRISPR/Cas9-mediated silencing of , we identified regulated expression of specific circular RNAs derived from (Titin), (Formin homology 2 domain containing 3), and (Striatin, calmodulin-binding protein 3). Moreover, inhibition of -derived circular RNA increased the susceptibility of cardiomyocytes to doxorubicin. We here show that overexpression of strongly attenuates the toxic effect of doxorubicin via regulating a set of circular RNAs. is, thus, an interesting target molecule to combat doxorubicin-induced cardiotoxicity.
RBPs (RNA-binding proteins) have been described to be expressed and regulated in various organs including the heart. Little is known about the role of RBPs in heart failure induced by the chemotherapy drug doxorubicin and their interaction with circular RNAs.RATIONALERBPs (RNA-binding proteins) have been described to be expressed and regulated in various organs including the heart. Little is known about the role of RBPs in heart failure induced by the chemotherapy drug doxorubicin and their interaction with circular RNAs.We aimed to identify key RBPs involved in doxorubicin-mediated heart failure and to elucidate their function.OBJECTIVEWe aimed to identify key RBPs involved in doxorubicin-mediated heart failure and to elucidate their function.Global transcriptome profiling from murine myocardium exposed to doxorubicin identified 5 differentially expressed RBPs. Expression of the RBP QKI (Quaking) in response to doxorubicin was strongly downregulated in rodent cardiomyocytes and human induced pluripotent stem cell-derived cardiomyocytes in vitro and in vivo in mice. Knockdown of Qki in primary cardiomyocytes increased apoptosis and atrophy after treatment with doxorubicin, whereas lentiviral mediated overexpression of Qki5 inhibited the doxorubicin-induced apoptosis in cardiomyocytes. In vivo, AAV9 (adeno-associated virus serotype 9)-mediated cardiac overexpression of Qki5 prevented cardiac apoptosis and cardiac atrophy induced by doxorubicin and improved cardiac function. Mechanistically, by lentiviral-based overexpression and CRISPR/Cas9-mediated silencing of Qki5, we identified regulated expression of specific circular RNAs derived from Ttn (Titin), Fhod3 (Formin homology 2 domain containing 3), and Strn3 (Striatin, calmodulin-binding protein 3). Moreover, inhibition of Ttn-derived circular RNA increased the susceptibility of cardiomyocytes to doxorubicin.METHODS AND RESULTSGlobal transcriptome profiling from murine myocardium exposed to doxorubicin identified 5 differentially expressed RBPs. Expression of the RBP QKI (Quaking) in response to doxorubicin was strongly downregulated in rodent cardiomyocytes and human induced pluripotent stem cell-derived cardiomyocytes in vitro and in vivo in mice. Knockdown of Qki in primary cardiomyocytes increased apoptosis and atrophy after treatment with doxorubicin, whereas lentiviral mediated overexpression of Qki5 inhibited the doxorubicin-induced apoptosis in cardiomyocytes. In vivo, AAV9 (adeno-associated virus serotype 9)-mediated cardiac overexpression of Qki5 prevented cardiac apoptosis and cardiac atrophy induced by doxorubicin and improved cardiac function. Mechanistically, by lentiviral-based overexpression and CRISPR/Cas9-mediated silencing of Qki5, we identified regulated expression of specific circular RNAs derived from Ttn (Titin), Fhod3 (Formin homology 2 domain containing 3), and Strn3 (Striatin, calmodulin-binding protein 3). Moreover, inhibition of Ttn-derived circular RNA increased the susceptibility of cardiomyocytes to doxorubicin.We here show that overexpression of Qki5 strongly attenuates the toxic effect of doxorubicin via regulating a set of circular RNAs. Qki5 is, thus, an interesting target molecule to combat doxorubicin-induced cardiotoxicity.CONCLUSIONSWe here show that overexpression of Qki5 strongly attenuates the toxic effect of doxorubicin via regulating a set of circular RNAs. Qki5 is, thus, an interesting target molecule to combat doxorubicin-induced cardiotoxicity.
Author Streckfuß-Bömeke, Katrin
Fiedler, Jan
Thum, Thomas
Milting, Hendrik
Gupta, Shashi Kumar
Garg, Ankita
Bär, Christian
Chatterjee, Shambhabi
Foinquinos, Ariana
Author_xml – sequence: 1
  givenname: Shashi Kumar
  surname: Gupta
  fullname: Gupta, Shashi Kumar
  email: gupta.shashi@mh-hannover.de, thum.thomas@mh-hannover.de
  organization: From the Institute of Molecular and Translational Therapeutic Strategies (S.K.G., A.G., C.B., S.C., A.F., J.F., T.T.) and Excellence Cluster REBIRTH (T.T.), Hannover Medical School, Germany; Herz- und Diabeteszentrum NRW, Universitätsklinikum der Ruhr Universität Bochum, Erich und Hanna Klessmann-Institute for Cardiovascular Research and Development, Bad Oeynhausen, Germany (H.M.); Clinic for Cardiology and Pneumology, Stem Cell Laboratory, University Medical Center, Gottingen, Germany (K.S.-B.); DZHK (German Center for Cardiovascular Research) Partner site Göttingen, Germany (K.S.-B.); and National Heart and Lung Institute, Imperial College London, United Kingdom (T.T.). gupta.shashi@mh-hannover.de thum.thomas@mh-hannover.de
– sequence: 2
  givenname: Ankita
  surname: Garg
  fullname: Garg, Ankita
  organization: From the Institute of Molecular and Translational Therapeutic Strategies (S.K.G., A.G., C.B., S.C., A.F., J.F., T.T.) and Excellence Cluster REBIRTH (T.T.), Hannover Medical School, Germany; Herz- und Diabeteszentrum NRW, Universitätsklinikum der Ruhr Universität Bochum, Erich und Hanna Klessmann-Institute for Cardiovascular Research and Development, Bad Oeynhausen, Germany (H.M.); Clinic for Cardiology and Pneumology, Stem Cell Laboratory, University Medical Center, Gottingen, Germany (K.S.-B.); DZHK (German Center for Cardiovascular Research) Partner site Göttingen, Germany (K.S.-B.); and National Heart and Lung Institute, Imperial College London, United Kingdom (T.T.)
– sequence: 3
  givenname: Christian
  surname: Bär
  fullname: Bär, Christian
  organization: From the Institute of Molecular and Translational Therapeutic Strategies (S.K.G., A.G., C.B., S.C., A.F., J.F., T.T.) and Excellence Cluster REBIRTH (T.T.), Hannover Medical School, Germany; Herz- und Diabeteszentrum NRW, Universitätsklinikum der Ruhr Universität Bochum, Erich und Hanna Klessmann-Institute for Cardiovascular Research and Development, Bad Oeynhausen, Germany (H.M.); Clinic for Cardiology and Pneumology, Stem Cell Laboratory, University Medical Center, Gottingen, Germany (K.S.-B.); DZHK (German Center for Cardiovascular Research) Partner site Göttingen, Germany (K.S.-B.); and National Heart and Lung Institute, Imperial College London, United Kingdom (T.T.)
– sequence: 4
  givenname: Shambhabi
  surname: Chatterjee
  fullname: Chatterjee, Shambhabi
  organization: From the Institute of Molecular and Translational Therapeutic Strategies (S.K.G., A.G., C.B., S.C., A.F., J.F., T.T.) and Excellence Cluster REBIRTH (T.T.), Hannover Medical School, Germany; Herz- und Diabeteszentrum NRW, Universitätsklinikum der Ruhr Universität Bochum, Erich und Hanna Klessmann-Institute for Cardiovascular Research and Development, Bad Oeynhausen, Germany (H.M.); Clinic for Cardiology and Pneumology, Stem Cell Laboratory, University Medical Center, Gottingen, Germany (K.S.-B.); DZHK (German Center for Cardiovascular Research) Partner site Göttingen, Germany (K.S.-B.); and National Heart and Lung Institute, Imperial College London, United Kingdom (T.T.)
– sequence: 5
  givenname: Ariana
  surname: Foinquinos
  fullname: Foinquinos, Ariana
  organization: From the Institute of Molecular and Translational Therapeutic Strategies (S.K.G., A.G., C.B., S.C., A.F., J.F., T.T.) and Excellence Cluster REBIRTH (T.T.), Hannover Medical School, Germany; Herz- und Diabeteszentrum NRW, Universitätsklinikum der Ruhr Universität Bochum, Erich und Hanna Klessmann-Institute for Cardiovascular Research and Development, Bad Oeynhausen, Germany (H.M.); Clinic for Cardiology and Pneumology, Stem Cell Laboratory, University Medical Center, Gottingen, Germany (K.S.-B.); DZHK (German Center for Cardiovascular Research) Partner site Göttingen, Germany (K.S.-B.); and National Heart and Lung Institute, Imperial College London, United Kingdom (T.T.)
– sequence: 6
  givenname: Hendrik
  surname: Milting
  fullname: Milting, Hendrik
  organization: From the Institute of Molecular and Translational Therapeutic Strategies (S.K.G., A.G., C.B., S.C., A.F., J.F., T.T.) and Excellence Cluster REBIRTH (T.T.), Hannover Medical School, Germany; Herz- und Diabeteszentrum NRW, Universitätsklinikum der Ruhr Universität Bochum, Erich und Hanna Klessmann-Institute for Cardiovascular Research and Development, Bad Oeynhausen, Germany (H.M.); Clinic for Cardiology and Pneumology, Stem Cell Laboratory, University Medical Center, Gottingen, Germany (K.S.-B.); DZHK (German Center for Cardiovascular Research) Partner site Göttingen, Germany (K.S.-B.); and National Heart and Lung Institute, Imperial College London, United Kingdom (T.T.)
– sequence: 7
  givenname: Katrin
  surname: Streckfuß-Bömeke
  fullname: Streckfuß-Bömeke, Katrin
  organization: From the Institute of Molecular and Translational Therapeutic Strategies (S.K.G., A.G., C.B., S.C., A.F., J.F., T.T.) and Excellence Cluster REBIRTH (T.T.), Hannover Medical School, Germany; Herz- und Diabeteszentrum NRW, Universitätsklinikum der Ruhr Universität Bochum, Erich und Hanna Klessmann-Institute for Cardiovascular Research and Development, Bad Oeynhausen, Germany (H.M.); Clinic for Cardiology and Pneumology, Stem Cell Laboratory, University Medical Center, Gottingen, Germany (K.S.-B.); DZHK (German Center for Cardiovascular Research) Partner site Göttingen, Germany (K.S.-B.); and National Heart and Lung Institute, Imperial College London, United Kingdom (T.T.)
– sequence: 8
  givenname: Jan
  surname: Fiedler
  fullname: Fiedler, Jan
  organization: From the Institute of Molecular and Translational Therapeutic Strategies (S.K.G., A.G., C.B., S.C., A.F., J.F., T.T.) and Excellence Cluster REBIRTH (T.T.), Hannover Medical School, Germany; Herz- und Diabeteszentrum NRW, Universitätsklinikum der Ruhr Universität Bochum, Erich und Hanna Klessmann-Institute for Cardiovascular Research and Development, Bad Oeynhausen, Germany (H.M.); Clinic for Cardiology and Pneumology, Stem Cell Laboratory, University Medical Center, Gottingen, Germany (K.S.-B.); DZHK (German Center for Cardiovascular Research) Partner site Göttingen, Germany (K.S.-B.); and National Heart and Lung Institute, Imperial College London, United Kingdom (T.T.)
– sequence: 9
  givenname: Thomas
  surname: Thum
  fullname: Thum, Thomas
  email: gupta.shashi@mh-hannover.de, thum.thomas@mh-hannover.de
  organization: From the Institute of Molecular and Translational Therapeutic Strategies (S.K.G., A.G., C.B., S.C., A.F., J.F., T.T.) and Excellence Cluster REBIRTH (T.T.), Hannover Medical School, Germany; Herz- und Diabeteszentrum NRW, Universitätsklinikum der Ruhr Universität Bochum, Erich und Hanna Klessmann-Institute for Cardiovascular Research and Development, Bad Oeynhausen, Germany (H.M.); Clinic for Cardiology and Pneumology, Stem Cell Laboratory, University Medical Center, Gottingen, Germany (K.S.-B.); DZHK (German Center for Cardiovascular Research) Partner site Göttingen, Germany (K.S.-B.); and National Heart and Lung Institute, Imperial College London, United Kingdom (T.T.). gupta.shashi@mh-hannover.de thum.thomas@mh-hannover.de
BackLink https://www.ncbi.nlm.nih.gov/pubmed/29133306$$D View this record in MEDLINE/PubMed
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Keywords heart failure
RNA-binding protein
cardiotoxicity
noncoding RNA
doxorubicin
Language English
License 2017 The Authors.
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PublicationTitle Circulation research
PublicationTitleAlternate Circ Res
PublicationYear 2018
References 29348242 - Circ Res. 2018 Jan 19;122(2):188-190
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Snippet RBPs (RNA-binding proteins) have been described to be expressed and regulated in various organs including the heart. Little is known about the role of RBPs in...
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SubjectTerms Animals
Antibiotics, Antineoplastic - toxicity
Cardiotoxicity - genetics
Cardiotoxicity - metabolism
Doxorubicin - toxicity
Gene Expression
Mice
Mice, Inbred C57BL
Myocytes, Cardiac - drug effects
Myocytes, Cardiac - metabolism
Random Allocation
RNA - biosynthesis
RNA - genetics
RNA-Binding Proteins - biosynthesis
RNA-Binding Proteins - genetics
Title Quaking Inhibits Doxorubicin-Mediated Cardiotoxicity Through Regulation of Cardiac Circular RNA Expression
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