Nejvíce citovaný článek - PubMed ID 9584831
The long (Gs(alpha)-L) and short (Gs(alpha)-S) variants of the stimulatory guanine nucleotide-binding protein. Do they behave in an identical way?
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.
- MeSH
- adenylátcyklasy genetika metabolismus MeSH
- exprese genu MeSH
- fluoridy farmakologie MeSH
- hypertrofie levé komory srdeční metabolismus MeSH
- isoprenalin farmakologie MeSH
- kardiomegalie genetika metabolismus patologie MeSH
- kardiotonika farmakologie MeSH
- kolforsin farmakologie MeSH
- krysa rodu Rattus MeSH
- mangan farmakologie MeSH
- myokard metabolismus MeSH
- novorozená zvířata * MeSH
- potkani Wistar MeSH
- protein - isoformy genetika metabolismus MeSH
- proteiny vázající GTP metabolismus MeSH
- signální transdukce MeSH
- stárnutí MeSH
- tlak * MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- srovnávací studie MeSH
- Názvy látek
- adenylátcyklasy MeSH
- fluoridy MeSH
- isoprenalin MeSH
- kardiotonika MeSH
- kolforsin MeSH
- mangan MeSH
- protein - isoformy MeSH
- proteiny vázající GTP MeSH