In Vivo Monitoring of Parathyroid Hormone Treatment after Myocardial Infarction in Mice with [Ga]Annexin A5 and [F]Fluorodeoxyglucose Positron Emission Tomography

[ 68 Ga]Annexin A5 positron emission tomography (PET) reveals the externalization of phosphatidylserine as a surrogate marker for apoptosis. We tested this technique for therapy monitoring in a murine model of myocardial infarction (MI) including parathyroid hormone (PTH) treatment. MI was induced i...

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Main Authors: Sebastian Lehner, Andrei Todica, Yordan Vanchev, Christopher Uebleis, Hao Wang, Tanja Herrler, Carmen Wängler, Paul Cumming, Guido Böning, Wolfgang M. Franz, Peter Bartenstein, Marcus Hacker, Stefan Brunner
Format: Article
Language:English
Published: SAGE Publications 2014-12-01
Series:Molecular Imaging
Online Access:https://doi.org/10.2310/7290.2014.00035
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author Sebastian Lehner
Andrei Todica
Yordan Vanchev
Christopher Uebleis
Hao Wang
Tanja Herrler
Carmen Wängler
Paul Cumming
Guido Böning
Wolfgang M. Franz
Peter Bartenstein
Marcus Hacker
Stefan Brunner
author_facet Sebastian Lehner
Andrei Todica
Yordan Vanchev
Christopher Uebleis
Hao Wang
Tanja Herrler
Carmen Wängler
Paul Cumming
Guido Böning
Wolfgang M. Franz
Peter Bartenstein
Marcus Hacker
Stefan Brunner
author_sort Sebastian Lehner
collection DOAJ
description [ 68 Ga]Annexin A5 positron emission tomography (PET) reveals the externalization of phosphatidylserine as a surrogate marker for apoptosis. We tested this technique for therapy monitoring in a murine model of myocardial infarction (MI) including parathyroid hormone (PTH) treatment. MI was induced in mice, and they were assigned to the saline or the PTH group. On day 2, they received [ 68 Ga]annexin A5 PET or histofluorescence TUNEL staining. Mice had 2-deoxy-2-[ 18 F]fluoro-D-glucose (FDG)-PET examinations on days 6 and 30 for calculation of the left ventricular ejection fraction and infarct area. [ 68 Ga]Annexin A5 uptake was 7.4 ± 1.3 %ID/g within the infarction for the controls and 4.5 ± 1.9 %ID/g for the PTH group ( p = .013). TUNEL staining revealed significantly more apoptotic cells in the infarct area on day 2 in the controls (64 ± 9%) compared to the treatment group (52 ± 4%; p = .045). FDG-PET revealed a significant decrease in infarct size in the treatment group and an increase in the controls. Examinations of left ventricular ejection fraction on days 6 and 30 did not reveal treatment effects. [ 68 Ga]Annexin A5 PET can detect the effects of PTH treatment as a marker of apoptosis 2 days after MI; ex vivo examination confirmed significant rescue of myocardiocytes. FDG-PET showed a small but significant reduction in infarct size but no functional improvement.
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spelling doaj.art-f9a409838b904a2da8ea60fe841316002024-03-02T00:29:08ZengSAGE PublicationsMolecular Imaging1536-01212014-12-011310.2310/7290.2014.0003510.2310_7290.2014.00035In Vivo Monitoring of Parathyroid Hormone Treatment after Myocardial Infarction in Mice with [Ga]Annexin A5 and [F]Fluorodeoxyglucose Positron Emission TomographySebastian LehnerAndrei TodicaYordan VanchevChristopher UebleisHao WangTanja HerrlerCarmen WänglerPaul CummingGuido BöningWolfgang M. FranzPeter BartensteinMarcus HackerStefan Brunner[ 68 Ga]Annexin A5 positron emission tomography (PET) reveals the externalization of phosphatidylserine as a surrogate marker for apoptosis. We tested this technique for therapy monitoring in a murine model of myocardial infarction (MI) including parathyroid hormone (PTH) treatment. MI was induced in mice, and they were assigned to the saline or the PTH group. On day 2, they received [ 68 Ga]annexin A5 PET or histofluorescence TUNEL staining. Mice had 2-deoxy-2-[ 18 F]fluoro-D-glucose (FDG)-PET examinations on days 6 and 30 for calculation of the left ventricular ejection fraction and infarct area. [ 68 Ga]Annexin A5 uptake was 7.4 ± 1.3 %ID/g within the infarction for the controls and 4.5 ± 1.9 %ID/g for the PTH group ( p = .013). TUNEL staining revealed significantly more apoptotic cells in the infarct area on day 2 in the controls (64 ± 9%) compared to the treatment group (52 ± 4%; p = .045). FDG-PET revealed a significant decrease in infarct size in the treatment group and an increase in the controls. Examinations of left ventricular ejection fraction on days 6 and 30 did not reveal treatment effects. [ 68 Ga]Annexin A5 PET can detect the effects of PTH treatment as a marker of apoptosis 2 days after MI; ex vivo examination confirmed significant rescue of myocardiocytes. FDG-PET showed a small but significant reduction in infarct size but no functional improvement.https://doi.org/10.2310/7290.2014.00035
spellingShingle Sebastian Lehner
Andrei Todica
Yordan Vanchev
Christopher Uebleis
Hao Wang
Tanja Herrler
Carmen Wängler
Paul Cumming
Guido Böning
Wolfgang M. Franz
Peter Bartenstein
Marcus Hacker
Stefan Brunner
In Vivo Monitoring of Parathyroid Hormone Treatment after Myocardial Infarction in Mice with [Ga]Annexin A5 and [F]Fluorodeoxyglucose Positron Emission Tomography
Molecular Imaging
title In Vivo Monitoring of Parathyroid Hormone Treatment after Myocardial Infarction in Mice with [Ga]Annexin A5 and [F]Fluorodeoxyglucose Positron Emission Tomography
title_full In Vivo Monitoring of Parathyroid Hormone Treatment after Myocardial Infarction in Mice with [Ga]Annexin A5 and [F]Fluorodeoxyglucose Positron Emission Tomography
title_fullStr In Vivo Monitoring of Parathyroid Hormone Treatment after Myocardial Infarction in Mice with [Ga]Annexin A5 and [F]Fluorodeoxyglucose Positron Emission Tomography
title_full_unstemmed In Vivo Monitoring of Parathyroid Hormone Treatment after Myocardial Infarction in Mice with [Ga]Annexin A5 and [F]Fluorodeoxyglucose Positron Emission Tomography
title_short In Vivo Monitoring of Parathyroid Hormone Treatment after Myocardial Infarction in Mice with [Ga]Annexin A5 and [F]Fluorodeoxyglucose Positron Emission Tomography
title_sort in vivo monitoring of parathyroid hormone treatment after myocardial infarction in mice with ga annexin a5 and f fluorodeoxyglucose positron emission tomography
url https://doi.org/10.2310/7290.2014.00035
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