Different onset of nucleolar activation in endocardial endothelial cells and cardiomyocytes following pressure overload in rat heart
Jazyk angličtina Země Anglie, Velká Británie Médium print
Typ dokumentu srovnávací studie, časopisecké články, práce podpořená grantem
PubMed
9299370
DOI
10.1006/jmcc.1997.0484
PII: S0022-2828(97)90484-3
Knihovny.cz E-zdroje
- MeSH
- aorta MeSH
- cévní endotel metabolismus MeSH
- endokard cytologie metabolismus MeSH
- genetická transkripce MeSH
- konstrikce MeSH
- krevní tlak * MeSH
- krysa rodu Rattus MeSH
- myokard cytologie metabolismus MeSH
- organizátor jadérka metabolismus MeSH
- potkani Wistar MeSH
- svaly hladké cévní cytologie metabolismus MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- srovnávací studie MeSH
We evaluated the time course of activation of endocardial endothelial cells and cardiomyocytes in adult rats with pressure overload induced by the abdominal aortic constriction. The silver staining technique for nucleolar organizer region was used to mark an increased transcriptional activity of the cells. An increased number of nucleoli was already detected in the endocardial endothelium of the left ventricle 5 h post-operatively, while the response of cardiomyocytes was still absent. Twenty-four h after constriction, the activation of the endocardial endothelium and cardiomyocytes was evident in both ventricles. A similar delay was observed between the nucleolar activation in vascular endothelium and smooth muscle cells of the abdominal aorta. In contrast, these cells of the thoracic aorta did not exhibit any significant increase of the transcriptional activity. The sequential stimulation of the transcriptional activity of the left ventricular endocardial endothelial cells and the subjacent cardiac myocytes due to pressure overload is in accord with the view that the endocardium may serve as a mechanotransducer which converts the hemodynamic changes into the signals that influence the growth of the cardiac myocytes.
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