| pubmed-article:7626007 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7626007 | lifeskim:mentions | umls-concept:C0043167 | lld:lifeskim |
| pubmed-article:7626007 | lifeskim:mentions | umls-concept:C0010453 | lld:lifeskim |
| pubmed-article:7626007 | lifeskim:mentions | umls-concept:C0225828 | lld:lifeskim |
| pubmed-article:7626007 | lifeskim:mentions | umls-concept:C1522565 | lld:lifeskim |
| pubmed-article:7626007 | lifeskim:mentions | umls-concept:C0752312 | lld:lifeskim |
| pubmed-article:7626007 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:7626007 | lifeskim:mentions | umls-concept:C1155502 | lld:lifeskim |
| pubmed-article:7626007 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:7626007 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:7626007 | pubmed:dateCreated | 1995-8-29 | lld:pubmed |
| pubmed-article:7626007 | pubmed:abstractText | The involvement of pertussis toxin (PTX)-sensitive and -insensitive pathways in the activation of the mitogen-activated protein kinase (MAPK) cascade was examined in ventricular cardiomyocytes cultured from neonatal rats. A number of agonists that activate heterotrimeric G-protein-coupled receptors stimulated MAPK activity after exposure for 5 min. These included foetal calf serum (FCS), endothelin-1 (these two being the most effective of the agonists examined), phenylephrine, endothelin-3, lysophosphatidic acid, carbachol, isoprenaline and angiotensin II. Activation of MAPK and MAPK kinase (MEK) by carbachol returned to control levels within 30-60 min, whereas activation by FCS was more sustained. FPLC on Mono Q showed that carbachol and FCS activated two peaks of MEK and two peaks of MAPK (p42MAPK and p44MAPK). Pretreatment of cells with PTX for 24 h inhibited the activation of MAPK by carbachol, FCS and lysophosphatidic acid, but not that by endothelin-1, phenylephrine or isoprenaline. Involvement of G-proteins in the activation of the cardiac MAPK cascade was demonstrated by the sustained (PTX-insensitive) activation of MAPK (and MEK) after exposure of cells to AlF4-. AlF4- activated PtdIns hydrolysis, as did endothelin-1, endothelin-3, phenylephrine and FCS. In contrast, the effect of lysophosphatidic acid on PtdIns hydrolysis was small and carbachol was without significant effect even after prolonged exposure. We conclude that PTX-sensitive (i.e. Gi/G(o)-linked) and PTX-insensitive (i.e. Gq/Gs-linked) pathways of MAPK activation exist in neonatal ventricular myocytes. FCS may stimulate the MAPK cascade through both pathways. | lld:pubmed |
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| pubmed-article:7626007 | pubmed:language | eng | lld:pubmed |
| pubmed-article:7626007 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7626007 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:7626007 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7626007 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:7626007 | pubmed:issn | 0264-6021 | lld:pubmed |
| pubmed-article:7626007 | pubmed:author | pubmed-author:SugdenP HPH | lld:pubmed |
| pubmed-article:7626007 | pubmed:author | pubmed-author:ClerkAA | lld:pubmed |
| pubmed-article:7626007 | pubmed:author | pubmed-author:BogoyevitchM... | lld:pubmed |
| pubmed-article:7626007 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7626007 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:7626007 | pubmed:volume | 309 ( Pt 2) | lld:pubmed |
| pubmed-article:7626007 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7626007 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7626007 | pubmed:pagination | 437-43 | lld:pubmed |
| pubmed-article:7626007 | pubmed:dateRevised | 2010-8-25 | lld:pubmed |
| pubmed-article:7626007 | pubmed:meshHeading | pubmed-meshheading:7626007-... | lld:pubmed |
| pubmed-article:7626007 | pubmed:meshHeading | pubmed-meshheading:7626007-... | lld:pubmed |
