Evidence map›Paper›PMID 19421833›Full record

ArticleBasic research in cardiology2009

Transcription profiling of HCN-channel isotypes throughout mouse cardiac development.

Patrick A Schweizer, Pessah Yampolsky, Rizwan Malik, Dierk Thomas, Joerg Zehelein, Hugo A Katus, Michael Koenen

Open access · hybridAbstract read
In one paragraph

Article in Basic research in cardiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.8field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 66 citations in OpenAlex.

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  11. Augmentation of myocardial INature communications · 2019
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  12. Article
  13. Age-associated expression of HCN channel isoforms in rat sinoatrial node.Experimental biology and medicine (Maywood, N.J.) · 2016
    Article
  14. Molecular Mapping of Sinoatrial Node HCN Channel Expression in the Human Heart.Circulation. Arrhythmia and electrophysiology · 2015
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 1 country.

Patrick A SchweizerUniversitätsklinikum Heidelberg, Innere Medizin III, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany.
Pessah Yampolsky
Rizwan Malik
Dierk Thomas
Joerg Zehelein
Hugo A Katus
Michael Koenen
Max Planck Institute for Medical Research · DEMax Planck Society · DEUniversity Hospital Heidelberg · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperpolarization-activated ion channels, encoded by four mammalian genes (HCN1-4), contribute in an important way to the cardiac pacemaker current I(f). 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.

Indexed as

AnimalsCyclic Nucleotide-Gated Cation ChannelsGene ExpressionGene Expression ProfilingHeartHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsIon ChannelsMiceMice, Inbred C57BLMyocardiumPotassium ChannelsPotassium Channels, Inwardly RectifyingPotassium Channels, Voltage-GatedReverse Transcriptase Polymerase Chain ReactionTranscription, GeneticCyclic Nucleotide-Gated Cation ChannelsHcn1 protein, mouseHcn2 protein, mouseHCN3 protein, mouseHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsIon ChannelsKcne2 protein, mouseKir2.1 channelPotassium ChannelsPotassium Channels, Inwardly RectifyingPotassium Channels, Voltage-Gated

Identifiers

PMID19421833
PMCPMC2758203
OpenAlexW1967153722

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.