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Evidence for a functional role of calsequestrin 2 in mouse atrium.

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Title: Evidence for a functional role of calsequestrin 2 in mouse atrium.
Authors: Gergs, U., Fahrion, C. M., Bock, P., Fischer, M., Wache, H., Hauptmann, S., Schmitz, W., Neumann, J.
Source: Acta Physiologica. Mar2017, Vol. 219 Issue 3, p669-684. 14p.
Subjects: Calsequestrin, Echocardiography, Animal models of arrhythmia, Heart function tests, Animal models in research, Heart diseases
Abstract: Aim Several genetically modified mice models were studied so far to investigate the role of cardiac calsequestrin (CSQ2) for the contractile function of the ventricle and for the occurrence of ventricular tachycardia. Using a CSQ2 knockout mouse, we wanted to study also the atrial function of CSQ2. Methods The influence of CSQ2 on atrial function and, for comparison, ventricular function was studied in isolated cardiac preparations and by echocardiography as well as electrocardiography in mice with deletion of CSQ2. Results Using deletion of exon 1, we have successfully generated a constitutive knockout mouse of the calsequestrin 2 gene (CSQ2−/−). CSQ2 protein was absent in the heart (atrium, ventricle), but also in oesophagus and skeletal muscle of homozygous knockout mice. In 6-month-old CSQ2−/− mice, relative left atrial weight was increased, whereas relative heart weight was unchanged. The staircase phenomena in paced left atrial preparations on force of contraction and the post-rest potentiation were different between wild type and CSQ2−/− indicative for a decreased sarcoplasmic Ca2+ load and supporting an important role of CSQ2 also in the atrium. The incidence of arrhythmias was increased in CSQ2−/−. In 2-year-old CSQ2−/− mice, cardiac hypertrophy and heart failure were noted possibly as a result of chronically increased cytosolic Ca2+ levels. Conclusion These data suggest a functional role of CSQ2 not only in the ventricle but also in the atrium of mammalian hearts. Loss of CSQ2 function can cause not only arrhythmias, but also cardiac hypertrophy and heart failure. [ABSTRACT FROM AUTHOR]
Copyright of Acta Physiologica is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: Evidence for a functional role of calsequestrin 2 in mouse atrium.
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  Data: <searchLink fieldCode="AR" term="%22Gergs%2C+U%2E%22">Gergs, U.</searchLink><br /><searchLink fieldCode="AR" term="%22Fahrion%2C+C%2E+M%2E%22">Fahrion, C. M.</searchLink><br /><searchLink fieldCode="AR" term="%22Bock%2C+P%2E%22">Bock, P.</searchLink><br /><searchLink fieldCode="AR" term="%22Fischer%2C+M%2E%22">Fischer, M.</searchLink><br /><searchLink fieldCode="AR" term="%22Wache%2C+H%2E%22">Wache, H.</searchLink><br /><searchLink fieldCode="AR" term="%22Hauptmann%2C+S%2E%22">Hauptmann, S.</searchLink><br /><searchLink fieldCode="AR" term="%22Schmitz%2C+W%2E%22">Schmitz, W.</searchLink><br /><searchLink fieldCode="AR" term="%22Neumann%2C+J%2E%22">Neumann, J.</searchLink>
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  Data: <searchLink fieldCode="JN" term="%22Acta+Physiologica%22">Acta Physiologica</searchLink>. Mar2017, Vol. 219 Issue 3, p669-684. 14p.
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  Data: <searchLink fieldCode="DE" term="%22Calsequestrin%22">Calsequestrin</searchLink><br /><searchLink fieldCode="DE" term="%22Echocardiography%22">Echocardiography</searchLink><br /><searchLink fieldCode="DE" term="%22Animal+models+of+arrhythmia%22">Animal models of arrhythmia</searchLink><br /><searchLink fieldCode="DE" term="%22Heart+function+tests%22">Heart function tests</searchLink><br /><searchLink fieldCode="DE" term="%22Animal+models+in+research%22">Animal models in research</searchLink><br /><searchLink fieldCode="DE" term="%22Heart+diseases%22">Heart diseases</searchLink>
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  Data: Aim Several genetically modified mice models were studied so far to investigate the role of cardiac calsequestrin (CSQ2) for the contractile function of the ventricle and for the occurrence of ventricular tachycardia. Using a CSQ2 knockout mouse, we wanted to study also the atrial function of CSQ2. Methods The influence of CSQ2 on atrial function and, for comparison, ventricular function was studied in isolated cardiac preparations and by echocardiography as well as electrocardiography in mice with deletion of CSQ2. Results Using deletion of exon 1, we have successfully generated a constitutive knockout mouse of the calsequestrin 2 gene (CSQ2−/−). CSQ2 protein was absent in the heart (atrium, ventricle), but also in oesophagus and skeletal muscle of homozygous knockout mice. In 6-month-old CSQ2−/− mice, relative left atrial weight was increased, whereas relative heart weight was unchanged. The staircase phenomena in paced left atrial preparations on force of contraction and the post-rest potentiation were different between wild type and CSQ2−/− indicative for a decreased sarcoplasmic Ca2+ load and supporting an important role of CSQ2 also in the atrium. The incidence of arrhythmias was increased in CSQ2−/−. In 2-year-old CSQ2−/− mice, cardiac hypertrophy and heart failure were noted possibly as a result of chronically increased cytosolic Ca2+ levels. Conclusion These data suggest a functional role of CSQ2 not only in the ventricle but also in the atrium of mammalian hearts. Loss of CSQ2 function can cause not only arrhythmias, but also cardiac hypertrophy and heart failure. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Acta Physiologica is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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      – SubjectFull: Animal models of arrhythmia
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              Text: Mar2017
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