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Redox Imaging Using Cardiac Myocyte-Specific Transgenic Biosensor Mice

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Redox Imaging Using Cardiac Myocyte-Specific Transgenic Biosensor Mice. / Swain, Lija; Kesemeyer, Andrea; Meyer-Roxlau, Stefanie; Vettel, Christiane; Zieseniss, Anke; Güntsch, Annemarie; Jatho, Aline; Becker, Andreas; Nanadikar, Maithily S.; Morgan, Bruce; Dennerlein, Sven; Shah, Ajay; El-Armouche, Ali; Nikolaev, Viacheslav O.; Katschinski, Dörthe M.

In: Circulation Research, Vol. 119, No. 9, 14.10.2016, p. 1004-1016.

Research output: Contribution to journalArticle

Harvard

Swain, L, Kesemeyer, A, Meyer-Roxlau, S, Vettel, C, Zieseniss, A, Güntsch, A, Jatho, A, Becker, A, Nanadikar, MS, Morgan, B, Dennerlein, S, Shah, A, El-Armouche, A, Nikolaev, VO & Katschinski, DM 2016, 'Redox Imaging Using Cardiac Myocyte-Specific Transgenic Biosensor Mice', Circulation Research, vol. 119, no. 9, pp. 1004-1016. https://doi.org/10.1161/CIRCRESAHA.116.309551

APA

Swain, L., Kesemeyer, A., Meyer-Roxlau, S., Vettel, C., Zieseniss, A., Güntsch, A., ... Katschinski, D. M. (2016). Redox Imaging Using Cardiac Myocyte-Specific Transgenic Biosensor Mice. Circulation Research, 119(9), 1004-1016. https://doi.org/10.1161/CIRCRESAHA.116.309551

Vancouver

Swain L, Kesemeyer A, Meyer-Roxlau S, Vettel C, Zieseniss A, Güntsch A et al. Redox Imaging Using Cardiac Myocyte-Specific Transgenic Biosensor Mice. Circulation Research. 2016 Oct 14;119(9):1004-1016. https://doi.org/10.1161/CIRCRESAHA.116.309551

Author

Swain, Lija ; Kesemeyer, Andrea ; Meyer-Roxlau, Stefanie ; Vettel, Christiane ; Zieseniss, Anke ; Güntsch, Annemarie ; Jatho, Aline ; Becker, Andreas ; Nanadikar, Maithily S. ; Morgan, Bruce ; Dennerlein, Sven ; Shah, Ajay ; El-Armouche, Ali ; Nikolaev, Viacheslav O. ; Katschinski, Dörthe M. / Redox Imaging Using Cardiac Myocyte-Specific Transgenic Biosensor Mice. In: Circulation Research. 2016 ; Vol. 119, No. 9. pp. 1004-1016.

Bibtex Download

@article{5ac9bb0a0163459389425c76ac38d258,
title = "Redox Imaging Using Cardiac Myocyte-Specific Transgenic Biosensor Mice",
abstract = "Rationale: Changes in redox potentials of cardiac myocytes are linked to several cardiovascular diseases. Redox alterations are currently mostly described qualitatively using chemical sensors, which however do not allow quantifying redox potentials, lack specificity, and the possibility to analyze subcellular domains. Recent advances to quantitatively describe defined redox changes include the application of genetically encoded redox biosensors. Objective: Establishment of mouse models, which allow the quantification of the glutathione redox potential (E GSH) in the cytoplasm and the mitochondrial matrix of isolated cardiac myocytes and in Langendorff-perfused hearts based on the use of the redox-sensitive green fluorescent protein 2, coupled to the glutaredoxin 1 (Grx1-roGFP2). Methods and Results: We generated transgenic mice with cardiac myocyte-restricted expression of Grx1-roGFP2 targeted either to the mitochondrial matrix or to the cytoplasm. The response of the roGFP2 toward H2O2, diamide, and dithiothreitol was titrated and used to determine the E GSH in isolated cardiac myocytes and in Langendorff-perfused hearts. Distinct E GSH were observed in the cytoplasm and the mitochondrial matrix. Stimulation of the cardiac myocytes with isoprenaline, angiotensin II, or exposure to hypoxia/reoxygenation additionally underscored that these compartments responded independently. A compartment-specific response was also observed 3 to 14 days after myocardial infarction. Conclusions: We introduce redox biosensor mice as a new tool, which allows quantification of defined alterations of E GSH in the cytoplasm and the mitochondrial matrix in cardiac myocytes and can be exploited to answer questions in basic and translational cardiovascular research.",
keywords = "angiotensin II, cytoplasm, diamide, ischemia, reactive oxygen species",
author = "Lija Swain and Andrea Kesemeyer and Stefanie Meyer-Roxlau and Christiane Vettel and Anke Zieseniss and Annemarie G{\"u}ntsch and Aline Jatho and Andreas Becker and Nanadikar, {Maithily S.} and Bruce Morgan and Sven Dennerlein and Ajay Shah and Ali El-Armouche and Nikolaev, {Viacheslav O.} and Katschinski, {D{\"o}rthe M.}",
year = "2016",
month = "10",
day = "14",
doi = "10.1161/CIRCRESAHA.116.309551",
language = "English",
volume = "119",
pages = "1004--1016",
journal = "Circulation Research",
issn = "0009-7330",
publisher = "Lippincott Williams and Wilkins",
number = "9",

}

RIS (suitable for import to EndNote) Download

TY - JOUR

T1 - Redox Imaging Using Cardiac Myocyte-Specific Transgenic Biosensor Mice

AU - Swain, Lija

AU - Kesemeyer, Andrea

AU - Meyer-Roxlau, Stefanie

AU - Vettel, Christiane

AU - Zieseniss, Anke

AU - Güntsch, Annemarie

AU - Jatho, Aline

AU - Becker, Andreas

AU - Nanadikar, Maithily S.

AU - Morgan, Bruce

AU - Dennerlein, Sven

AU - Shah, Ajay

AU - El-Armouche, Ali

AU - Nikolaev, Viacheslav O.

AU - Katschinski, Dörthe M.

PY - 2016/10/14

Y1 - 2016/10/14

N2 - Rationale: Changes in redox potentials of cardiac myocytes are linked to several cardiovascular diseases. Redox alterations are currently mostly described qualitatively using chemical sensors, which however do not allow quantifying redox potentials, lack specificity, and the possibility to analyze subcellular domains. Recent advances to quantitatively describe defined redox changes include the application of genetically encoded redox biosensors. Objective: Establishment of mouse models, which allow the quantification of the glutathione redox potential (E GSH) in the cytoplasm and the mitochondrial matrix of isolated cardiac myocytes and in Langendorff-perfused hearts based on the use of the redox-sensitive green fluorescent protein 2, coupled to the glutaredoxin 1 (Grx1-roGFP2). Methods and Results: We generated transgenic mice with cardiac myocyte-restricted expression of Grx1-roGFP2 targeted either to the mitochondrial matrix or to the cytoplasm. The response of the roGFP2 toward H2O2, diamide, and dithiothreitol was titrated and used to determine the E GSH in isolated cardiac myocytes and in Langendorff-perfused hearts. Distinct E GSH were observed in the cytoplasm and the mitochondrial matrix. Stimulation of the cardiac myocytes with isoprenaline, angiotensin II, or exposure to hypoxia/reoxygenation additionally underscored that these compartments responded independently. A compartment-specific response was also observed 3 to 14 days after myocardial infarction. Conclusions: We introduce redox biosensor mice as a new tool, which allows quantification of defined alterations of E GSH in the cytoplasm and the mitochondrial matrix in cardiac myocytes and can be exploited to answer questions in basic and translational cardiovascular research.

AB - Rationale: Changes in redox potentials of cardiac myocytes are linked to several cardiovascular diseases. Redox alterations are currently mostly described qualitatively using chemical sensors, which however do not allow quantifying redox potentials, lack specificity, and the possibility to analyze subcellular domains. Recent advances to quantitatively describe defined redox changes include the application of genetically encoded redox biosensors. Objective: Establishment of mouse models, which allow the quantification of the glutathione redox potential (E GSH) in the cytoplasm and the mitochondrial matrix of isolated cardiac myocytes and in Langendorff-perfused hearts based on the use of the redox-sensitive green fluorescent protein 2, coupled to the glutaredoxin 1 (Grx1-roGFP2). Methods and Results: We generated transgenic mice with cardiac myocyte-restricted expression of Grx1-roGFP2 targeted either to the mitochondrial matrix or to the cytoplasm. The response of the roGFP2 toward H2O2, diamide, and dithiothreitol was titrated and used to determine the E GSH in isolated cardiac myocytes and in Langendorff-perfused hearts. Distinct E GSH were observed in the cytoplasm and the mitochondrial matrix. Stimulation of the cardiac myocytes with isoprenaline, angiotensin II, or exposure to hypoxia/reoxygenation additionally underscored that these compartments responded independently. A compartment-specific response was also observed 3 to 14 days after myocardial infarction. Conclusions: We introduce redox biosensor mice as a new tool, which allows quantification of defined alterations of E GSH in the cytoplasm and the mitochondrial matrix in cardiac myocytes and can be exploited to answer questions in basic and translational cardiovascular research.

KW - angiotensin II

KW - cytoplasm

KW - diamide

KW - ischemia

KW - reactive oxygen species

UR - http://www.scopus.com/inward/record.url?scp=84984704751&partnerID=8YFLogxK

U2 - 10.1161/CIRCRESAHA.116.309551

DO - 10.1161/CIRCRESAHA.116.309551

M3 - Article

C2 - 27553648

AN - SCOPUS:84984704751

VL - 119

SP - 1004

EP - 1016

JO - Circulation Research

JF - Circulation Research

SN - 0009-7330

IS - 9

ER -

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