Linked Life Data

12708755

Source:http://linkedlifedata.com/resource/pubmed/id/12708755

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2003-4-23
pubmed:abstractText
G proteins-coupled signaling pathways appear to play a role in the development of cardiac hypertrophy and its progression to heart failure. The present study aimed to investigate trimeric G proteins and adenylyl cyclase signaling in immature as well as in adult rat myocardium during this process caused by pressure overload. Pressure overload was induced in newborn (2-day-old) rats by abdominal aortic banding and myocardial preparations from left ventricular myocardium of immature (10-day-old) and adult (90-day-old) animals were analyzed for the relative content of different G protein subunits and adenylyl cyclase (AC) by immunoblotting with specific antibodies. A functional status of the AC signaling system was also evaluated. Normal maturation of rat heart was accompanied by increased expression of AC type V/VI and VII and of the long isoform (G(s)alphaL) of G(s)alpha protein. In parallel, the amounts of myocardial G(i)alpha/G(o)alpha proteins tended to decrease, and G(q)alpha/G(11)alpha and Gbeta did not change. Interestingly, whereas fluoride-stimulated AC activity increased in the course of maturation, activity of AC measured under other experimental conditions (stimulation by Mn2+, forskolin or isoproterenol) was lower in adult than in young rat myocardium. Pressure overload did not influence distribution of G proteins in immature myocardium, but considerably decreased the content of G(s)alphaL and increased G(o)alpha proteins in hearts of 90-day-old rats. These hearts exhibited worsened functional reserve as compared to age-matched controls and activity of AC was also markedly lower. A considerable reduction in Mn(2+)-stimulated AC activity together with similar decrease in AC activity determined under other stimulation conditions suggests that it is a function of AC catalytic subunit that is primarily impaired in this model of pressure overload.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0300-8177
pubmed:author
pubmed:issnType
Print
pubmed:volume
245
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
157-66
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:12708755-Adenylate Cyclase, pubmed-meshheading:12708755-Aging, pubmed-meshheading:12708755-Animals, pubmed-meshheading:12708755-Animals, Newborn, pubmed-meshheading:12708755-Cardiomegaly, pubmed-meshheading:12708755-Cardiotonic Agents, pubmed-meshheading:12708755-Fluorides, pubmed-meshheading:12708755-Forskolin, pubmed-meshheading:12708755-GTP-Binding Proteins, pubmed-meshheading:12708755-Gene Expression, pubmed-meshheading:12708755-Hypertrophy, Left Ventricular, pubmed-meshheading:12708755-Isoproterenol, pubmed-meshheading:12708755-Manganese, pubmed-meshheading:12708755-Myocardium, pubmed-meshheading:12708755-Pressure, pubmed-meshheading:12708755-Protein Isoforms, pubmed-meshheading:12708755-Rats, pubmed-meshheading:12708755-Rats, Wistar, pubmed-meshheading:12708755-Signal Transduction
pubmed:year
2003
pubmed:articleTitle
Cardiomegaly induced by pressure overload in newborn rats is accompanied by altered expression of the long isoform of G(s)alpha protein and deranged signaling of adenylyl cyclase.
pubmed:affiliation
Department of Physiology and Developmental Biology, Faculty of Natural Sciences, Charles University, Prague, Czech Republic. novjiri@biomed.cas.cz
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't