Linked Life Data

16041620

Source:http://linkedlifedata.com/resource/pubmed/id/16041620

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2005-7-25
pubmed:abstractText
The hypoxia-inducible factor (HIF)-1 is a master transcriptional activator of oxygen-regulated genes involved in energy metabolism, angiogenesis, and erythropoiesis. HIF-1 is composed of the two subunits HIF-1alpha and HIF-1beta (also called ARNT). The destruction of HIF-1alpha in the presence of oxygen is initiated by prolyl-4-hydroxylation. In human cells three closely related prolyl hydroxylases (PHDs) have been identified. An age-dependent decrease in HIF-1alpha expression was reported previously in brain, liver and kidney, which may be associated with a reduced adaptation to hypoxia as found in aged animals and humans. We have determined the expression of HIF-1alpha and the PHDs in human atrial trabeculae under normoxic and hypoxic conditions, in samples of human left ventricles as well as in heart extracts from female mice of different age (5 up to 16 months). With increasing age we found a decreased expression of HIF-1alpha, which correlated to an increased PHD3 expression in mouse and human heart. PHD3 was the most prominent HIF modifying hydroxylase found in human heart samples. Additionally, we found a strong ischemia/hypoxia-inducibility of PHD3 compared to PHD1 and PHD2 in atrial trabeculae. These data may explain the previously reported reduction of HIF-1alpha and HIF-1 target genes such as the vascular endothelial growth factor in ageing tissue.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1389-5729
pubmed:author
pubmed:issnType
Print
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
165-71
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Age-dependent increase of prolyl-4-hydroxylase domain (PHD) 3 expression in human and mouse heart.
pubmed:affiliation
Institute of Pathophysiology, Martin-Luther University Halle, Germany.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't