Contractility of myofibrils from the heart and diaphragm muscles measured with atomic force cantilevers : effects of heart-specific deletion of arginyl-tRNA-protein transferase
Copyright © 2013 Elsevier Ireland Ltd. All rights reserved..
BACKGROUND: Contractile properties of myofibrils from the myocardium and diaphragm in chronic heart failure are not well understood. We investigated myofibrils in a knockout (KO) mouse model with cardiac-specific deletion of arginyl-tRNA-protein transferase (α-MHCAte1), which presents dilated cardiomyopathy and heart failure.
OBJECTIVE: The aim of this study was to test the hypothesis that chronic heart failure in α-MHCAte1 mice is associated with abnormal contractile properties of the heart and diaphragm.
METHODS: We used a newly developed system of atomic force cantilevers (AFC) to compare myofibrils from α-MHCAte1 and age-matched wild type mice (WT). Myofibrils from the myocardium and the diaphragm were attached to the AFC used for force measurements during activation/deactivation cycles at different sarcomere lengths.
RESULTS: In the heart, α-MHCAte1 myofibrils presented a reduced force during full activation (89±9 nN/μm(2)) when compared to WT (132±11 nN/μm(2)), and the decrease was not influenced by sarcomere length. These myofibrils presented similar kinetics of force development (K(act)), redevelopment (K(tr)), and relaxation (K(rel)). In the diaphragm, α-MHCAte1 myofibrils presented an increased force during full activation (209±31 nN/μm(2)) when compared to WT (123±20 nN/μm(2)). Diaphragm myofibrils of α-MHCAte1 and WT presented similar K(act), but α-MHCAte1 myofibrils presented a faster K(rel) (6.11±0.41s(-1) vs 4.63±0.41 s(-1)).
CONCLUSION: Contrary to our working hypothesis, diaphragm myofibrils from α-MHCAte1 mice produced an increased force compared to myofibrils from WT. These results suggest a potential compensatory mechanism by which the diaphragm works under loading conditions in the α-MHCAte1 chronic heart failure model.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2013 |
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| Erschienen: |
2013 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:168 |
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| Enthalten in: |
International journal of cardiology - 168(2013), 4 vom: 09. Okt., Seite 3564-71 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Ribeiro, Paula A B [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 26.06.2014 Date Revised 21.10.2013 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1016/j.ijcard.2013.05.069 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM228094011 |
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| 041 | |a eng | ||
| 100 | 1 | |a Ribeiro, Paula A B |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Contractility of myofibrils from the heart and diaphragm muscles measured with atomic force cantilevers |b effects of heart-specific deletion of arginyl-tRNA-protein transferase |
| 264 | 1 | |c 2013 | |
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| 500 | |a Date Completed 26.06.2014 | ||
| 500 | |a Date Revised 21.10.2013 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Copyright © 2013 Elsevier Ireland Ltd. All rights reserved. | ||
| 520 | |a BACKGROUND: Contractile properties of myofibrils from the myocardium and diaphragm in chronic heart failure are not well understood. We investigated myofibrils in a knockout (KO) mouse model with cardiac-specific deletion of arginyl-tRNA-protein transferase (α-MHCAte1), which presents dilated cardiomyopathy and heart failure | ||
| 520 | |a OBJECTIVE: The aim of this study was to test the hypothesis that chronic heart failure in α-MHCAte1 mice is associated with abnormal contractile properties of the heart and diaphragm | ||
| 520 | |a METHODS: We used a newly developed system of atomic force cantilevers (AFC) to compare myofibrils from α-MHCAte1 and age-matched wild type mice (WT). Myofibrils from the myocardium and the diaphragm were attached to the AFC used for force measurements during activation/deactivation cycles at different sarcomere lengths | ||
| 520 | |a RESULTS: In the heart, α-MHCAte1 myofibrils presented a reduced force during full activation (89±9 nN/μm(2)) when compared to WT (132±11 nN/μm(2)), and the decrease was not influenced by sarcomere length. These myofibrils presented similar kinetics of force development (K(act)), redevelopment (K(tr)), and relaxation (K(rel)). In the diaphragm, α-MHCAte1 myofibrils presented an increased force during full activation (209±31 nN/μm(2)) when compared to WT (123±20 nN/μm(2)). Diaphragm myofibrils of α-MHCAte1 and WT presented similar K(act), but α-MHCAte1 myofibrils presented a faster K(rel) (6.11±0.41s(-1) vs 4.63±0.41 s(-1)) | ||
| 520 | |a CONCLUSION: Contrary to our working hypothesis, diaphragm myofibrils from α-MHCAte1 mice produced an increased force compared to myofibrils from WT. These results suggest a potential compensatory mechanism by which the diaphragm works under loading conditions in the α-MHCAte1 chronic heart failure model | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, N.I.H., Extramural | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a Arginylation | |
| 650 | 4 | |a Atomic force cantilever | |
| 650 | 4 | |a Cardiomyopathy | |
| 650 | 4 | |a Myofibrils | |
| 650 | 7 | |a Aminoacyltransferases |2 NLM | |
| 650 | 7 | |a EC 2.3.2.- |2 NLM | |
| 650 | 7 | |a arginyltransferase |2 NLM | |
| 650 | 7 | |a EC 2.3.2.8 |2 NLM | |
| 700 | 1 | |a Ribeiro, Jorge P |e verfasserin |4 aut | |
| 700 | 1 | |a Minozzo, Fábio C |e verfasserin |4 aut | |
| 700 | 1 | |a Pavlov, Ivan |e verfasserin |4 aut | |
| 700 | 1 | |a Leu, Nicolae A |e verfasserin |4 aut | |
| 700 | 1 | |a Kurosaka, Satoshi |e verfasserin |4 aut | |
| 700 | 1 | |a Kashina, Anna |e verfasserin |4 aut | |
| 700 | 1 | |a Rassier, Dilson E |e verfasserin |4 aut | |
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