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  Transcription profiling of HCN-channel isotypes throughout mouse cardiac development

Schweizer, P., Yampolsky, P., Malik, R., Thomas, D., Zehelein, J., Katus, H. A., et al. (2009). Transcription profiling of HCN-channel isotypes throughout mouse cardiac development. Basic Research in Cardiology, 104(6), 621-629. doi:10.1007/s00395-009-0031-5.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-002C-15F3-A Version Permalink: http://hdl.handle.net/21.11116/0000-0000-DED9-2
Genre: Journal Article

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BasicResCardiol_104_2009_621.pdf (Any fulltext), 271KB
 
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 Creators:
Schweizer, Patrick1, Author              
Yampolsky, Pessah1, Author              
Malik, Rizwan1, Author              
Thomas, Dierck, Author
Zehelein, Joerg1, Author              
Katus, Hugo A., Author
Koenen, Michael1, Author              
Affiliations:
1Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497704              

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Free keywords: Hyperpolarization; activated ion channels; Pacemaker channels; Gene expression; Sinoatrial node; Transcription; Developmental biology
 Abstract: Hyperpolarization-activated ion channels, encoded by four mammalian genes (HCN1-4), contribute in an important way to the cardiac pacemaker current If. Here, we describe the transcription profiles of the four HCN genes, the NRSF, KCNE2 and Kir2.1 genes from embryonic stage E9.5 dpc to postnatal day 120 in the mouse. Embryonic atrium and ventricle revealed abundant HCN4 transcription but other HCN transcripts were almost absent. Towards birth, HCN4 was downregulated in the atrium and almost vanished from the ventricle. After birth, however, HCN isotype transcription changed remarkably, showing increased levels of HCN1, HCN2 and HCN4 in the atrium and of HCN2 and HCN4 in the ventricle. HCN3 showed highest transcription at early embryonic stages and was hardly detectable thereafter. At postnatal day 10, HCN4 was highest in the sinoatrial node, being twofold higher than HCN1 and fivefold higher than HCN2. In the atrium, HCN4 was similar to HCN1 and sevenfold higher than HCN2. In the ventricle, in contrast, HCN2 was sixfold higher than HCN4, while HCN1 was absent. Subsequently all HCN isotype transcripts declined to lower adult levels, while ratios of HCN isotypes remained stable. In conclusion, substantial changes of HCN isotype transcription throughout cardiac development suggest that a regulated pattern of HCN isotypes is required to establish and ensure a stable heart rhythm. Furthermore, constantly low HCN transcription in adult myocardium may be required to prevent atrial and ventricular arrhythmogenesis.

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Language(s): eng - English
 Dates: 2008-12-012009-04-222009-05-072009-11
 Publication Status: Published in print
 Pages: 9
 Publishing info: -
 Table of Contents: -
 Rev. Method: Peer
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Title: Basic Research in Cardiology
  Other : Basic Res. Cardiol.
Source Genre: Journal
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Publ. Info: Darmstadt : D. Steinkopff.
Pages: - Volume / Issue: 104 (6) Sequence Number: - Start / End Page: 621 - 629 Identifier: ISSN: 0300-8428
CoNE: https://pure.mpg.de/cone/journals/resource/954927519611