Analysis of Tyrosine Kinase Inhibitor-Mediated Decline in Contractile Force in Rat Engineered Heart Tissue.

<h4>Introduction</h4>Left ventricular dysfunction is a frequent and potentially severe side effect of many tyrosine kinase inhibitors (TKI). The mode of toxicity is not identified, but may include impairment of mitochondrial or sarcomeric function, autophagy or angiogenesis, either as an...

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Main Authors: Fabian Jacob, Amina Y Yonis, Friederike Cuello, Pradeep Luther, Thomas Schulze, Alexandra Eder, Thomas Streichert, Ingra Mannhardt, Marc N Hirt, Sebastian Schaaf, Justus Stenzig, Thomas Force, Thomas Eschenhagen, Arne Hansen
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2016-01-01
Series:PLoS ONE
Online Access:https://doi.org/10.1371/journal.pone.0145937
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author Fabian Jacob
Amina Y Yonis
Friederike Cuello
Pradeep Luther
Thomas Schulze
Alexandra Eder
Thomas Streichert
Ingra Mannhardt
Marc N Hirt
Sebastian Schaaf
Justus Stenzig
Thomas Force
Thomas Eschenhagen
Arne Hansen
author_facet Fabian Jacob
Amina Y Yonis
Friederike Cuello
Pradeep Luther
Thomas Schulze
Alexandra Eder
Thomas Streichert
Ingra Mannhardt
Marc N Hirt
Sebastian Schaaf
Justus Stenzig
Thomas Force
Thomas Eschenhagen
Arne Hansen
author_sort Fabian Jacob
collection DOAJ
description <h4>Introduction</h4>Left ventricular dysfunction is a frequent and potentially severe side effect of many tyrosine kinase inhibitors (TKI). The mode of toxicity is not identified, but may include impairment of mitochondrial or sarcomeric function, autophagy or angiogenesis, either as an on-target or off-target mechanism.<h4>Methods and results</h4>We studied concentration-response curves and time courses for nine TKIs in three-dimensional, force generating engineered heart tissue (EHT) from neonatal rat heart cells. We detected a concentration- and time-dependent decline in contractile force for gefitinib, lapatinib, sunitinib, imatinib, sorafenib, vandetanib and lestaurtinib and no decline in contractile force for erlotinib and dasatinib after 96 hours of incubation. The decline in contractile force was associated with an impairment of autophagy (LC3 Western blot) and appearance of autophagolysosomes (transmission electron microscopy).<h4>Conclusion</h4>This study demonstrates the feasibility to study TKI-mediated force effects in EHTs and identifies an association between a decline in contractility and inhibition of autophagic flux.
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spelling doaj-art-4f66960b03bb435d9932d201d933a2ed2025-08-20T02:34:07ZengPublic Library of Science (PLoS)PLoS ONE1932-62032016-01-01112e014593710.1371/journal.pone.0145937Analysis of Tyrosine Kinase Inhibitor-Mediated Decline in Contractile Force in Rat Engineered Heart Tissue.Fabian JacobAmina Y YonisFriederike CuelloPradeep LutherThomas SchulzeAlexandra EderThomas StreichertIngra MannhardtMarc N HirtSebastian SchaafJustus StenzigThomas ForceThomas EschenhagenArne Hansen<h4>Introduction</h4>Left ventricular dysfunction is a frequent and potentially severe side effect of many tyrosine kinase inhibitors (TKI). The mode of toxicity is not identified, but may include impairment of mitochondrial or sarcomeric function, autophagy or angiogenesis, either as an on-target or off-target mechanism.<h4>Methods and results</h4>We studied concentration-response curves and time courses for nine TKIs in three-dimensional, force generating engineered heart tissue (EHT) from neonatal rat heart cells. We detected a concentration- and time-dependent decline in contractile force for gefitinib, lapatinib, sunitinib, imatinib, sorafenib, vandetanib and lestaurtinib and no decline in contractile force for erlotinib and dasatinib after 96 hours of incubation. The decline in contractile force was associated with an impairment of autophagy (LC3 Western blot) and appearance of autophagolysosomes (transmission electron microscopy).<h4>Conclusion</h4>This study demonstrates the feasibility to study TKI-mediated force effects in EHTs and identifies an association between a decline in contractility and inhibition of autophagic flux.https://doi.org/10.1371/journal.pone.0145937
spellingShingle Fabian Jacob
Amina Y Yonis
Friederike Cuello
Pradeep Luther
Thomas Schulze
Alexandra Eder
Thomas Streichert
Ingra Mannhardt
Marc N Hirt
Sebastian Schaaf
Justus Stenzig
Thomas Force
Thomas Eschenhagen
Arne Hansen
Analysis of Tyrosine Kinase Inhibitor-Mediated Decline in Contractile Force in Rat Engineered Heart Tissue.
PLoS ONE
title Analysis of Tyrosine Kinase Inhibitor-Mediated Decline in Contractile Force in Rat Engineered Heart Tissue.
title_full Analysis of Tyrosine Kinase Inhibitor-Mediated Decline in Contractile Force in Rat Engineered Heart Tissue.
title_fullStr Analysis of Tyrosine Kinase Inhibitor-Mediated Decline in Contractile Force in Rat Engineered Heart Tissue.
title_full_unstemmed Analysis of Tyrosine Kinase Inhibitor-Mediated Decline in Contractile Force in Rat Engineered Heart Tissue.
title_short Analysis of Tyrosine Kinase Inhibitor-Mediated Decline in Contractile Force in Rat Engineered Heart Tissue.
title_sort analysis of tyrosine kinase inhibitor mediated decline in contractile force in rat engineered heart tissue
url https://doi.org/10.1371/journal.pone.0145937
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