Linked Life Data

16985003

Source:http://linkedlifedata.com/resource/pubmed/id/16985003

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2007-2-13
pubmed:abstractText
The immature and mature heart differ from each other in terms of excitability, action potential properties, contractility, and relaxation. This includes upregulation of repolarizing K(+) currents, an enhanced inward rectifier K(+) (Kir) current, and changes in Ca(2+), Na(+), and Cl(-) currents. At the molecular level, the developmental regulation of ion channels is scantily described. Using a large-scale real-time quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) assay, we performed a comprehensive analysis of ion channel transcript expression during perinatal development in the embryonic (embryonic day 17.5), neonatal (postnatal days 1-2), and adult Swiss-Webster mouse hearts. These data are compared with publicly available microarray data sets (Cardiogenomics project). Developmental mRNA expression for several transcripts was consistent with the published literature. For example, transcripts such as Kir2.1, Kir3.1, Nav1.5, Cav1.2, etc. were upregulated after birth, whereas others [e.g., Ca(2+)-activated K(+) (KCa)2.3 and minK] were downregulated. Cl(-) channel transcripts were expressed at higher levels in immature heart, particularly those that are activated by intracellular Ca(2+). Defining alterations in the ion channel transcriptome during perinatal development will lead to a much improved understanding of the electrophysiological alterations occurring in the heart after birth. Our study may have important repercussions in understanding the mechanisms and consequences of electrophysiological alterations in infants and may pave the way for better understanding of clinically relevant events such as congenital abnormalities, cardiomyopathies, heart failure, arrhythmias, cardiac drug therapy, and the sudden infant death syndrome.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1531-2267
pubmed:author
pubmed:issnType
Electronic
pubmed:day
12
pubmed:volume
28
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
273-83
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:16985003-Animals, pubmed-meshheading:16985003-Calcium Channels, pubmed-meshheading:16985003-Chloride Channels, pubmed-meshheading:16985003-Cyclic Nucleotide-Gated Cation Channels, pubmed-meshheading:16985003-Gene Expression, pubmed-meshheading:16985003-Heart, pubmed-meshheading:16985003-Ion Channels, pubmed-meshheading:16985003-Mice, pubmed-meshheading:16985003-Mice, Transgenic, pubmed-meshheading:16985003-Myocardium, pubmed-meshheading:16985003-Potassium Channels, pubmed-meshheading:16985003-Potassium Channels, Calcium-Activated, pubmed-meshheading:16985003-Potassium Channels, Inwardly Rectifying, pubmed-meshheading:16985003-Protein Array Analysis, pubmed-meshheading:16985003-RNA, Messenger, pubmed-meshheading:16985003-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:16985003-Sodium Channels
pubmed:year
2007
pubmed:articleTitle
Large-scale analysis of ion channel gene expression in the mouse heart during perinatal development.
pubmed:affiliation
Pediatric Cardiology, New York University School of Medicine, New York, New York 10016, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural