Details
| Originalsprache | Englisch |
|---|---|
| Seiten (von - bis) | 79-84 |
| Seitenumfang | 6 |
| Fachzeitschrift | Journal of Bioenergetics and Biomembranes |
| Jahrgang | 42 |
| Ausgabenummer | 1 |
| Publikationsstatus | Veröffentlicht - Feb. 2010 |
Abstract
The scrape-loading/dye transfer technique was applied on the bovine aortic endothelial cell line GM-7373 to analyze the effects of the antithrombolytic drug dipyridamole on gap junction coupling in endothelial cells. We found that a cell treatment for 24 h with dipyridamole in therapeutically relevant concentrations (1-100 microM) increased gap junction coupling in a dose dependent manner. Similar to dipyridamole, forskolin as well as 8-Br-cAMP increased the gap junction coupling, while dibutyryl-cGMP (db-cGMP) did not affect the gap junction coupling of the GM-7373 endothelial cells. In parallel, a pharmacological inhibition of protein kinase A (PKA) with N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide dihydrochloride (H-89), antagonised the action of dipyridamole on gap junction coupling. We propose that the observed dipyridamole induced increase in gap junction coupling in endothelial cells is related to a cAMP-PKA dependent phosphorylation pathway. The report shows that gap junction coupling in endothelial cells is a suitable therapeutic target for treatment of cardiovascular diseases.
Ziele für nachhaltige Entwicklung
Zitieren
- Standard
- Harvard
- Apa
- Vancouver
- BibTex
- RIS
in: Journal of Bioenergetics and Biomembranes, Jahrgang 42, Nr. 1, 02.2010, S. 79-84.
Publikation: Beitrag in Fachzeitschrift › Artikel › Forschung › Peer-Review
}
TY - JOUR
T1 - Dipyridamole increases gap junction coupling in bovine GM-7373 aortic endothelial cells by a cAMP-protein kinase A dependent pathway
AU - Begandt, D
AU - Bintig, W
AU - Oberheide, K
AU - Schlie, S
AU - Ngezahayo, A
N1 - Funding information: The work was supported by Boehringer Ingel-heim International GmbH.
PY - 2010/2
Y1 - 2010/2
N2 - The scrape-loading/dye transfer technique was applied on the bovine aortic endothelial cell line GM-7373 to analyze the effects of the antithrombolytic drug dipyridamole on gap junction coupling in endothelial cells. We found that a cell treatment for 24 h with dipyridamole in therapeutically relevant concentrations (1-100 microM) increased gap junction coupling in a dose dependent manner. Similar to dipyridamole, forskolin as well as 8-Br-cAMP increased the gap junction coupling, while dibutyryl-cGMP (db-cGMP) did not affect the gap junction coupling of the GM-7373 endothelial cells. In parallel, a pharmacological inhibition of protein kinase A (PKA) with N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide dihydrochloride (H-89), antagonised the action of dipyridamole on gap junction coupling. We propose that the observed dipyridamole induced increase in gap junction coupling in endothelial cells is related to a cAMP-PKA dependent phosphorylation pathway. The report shows that gap junction coupling in endothelial cells is a suitable therapeutic target for treatment of cardiovascular diseases.
AB - The scrape-loading/dye transfer technique was applied on the bovine aortic endothelial cell line GM-7373 to analyze the effects of the antithrombolytic drug dipyridamole on gap junction coupling in endothelial cells. We found that a cell treatment for 24 h with dipyridamole in therapeutically relevant concentrations (1-100 microM) increased gap junction coupling in a dose dependent manner. Similar to dipyridamole, forskolin as well as 8-Br-cAMP increased the gap junction coupling, while dibutyryl-cGMP (db-cGMP) did not affect the gap junction coupling of the GM-7373 endothelial cells. In parallel, a pharmacological inhibition of protein kinase A (PKA) with N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide dihydrochloride (H-89), antagonised the action of dipyridamole on gap junction coupling. We propose that the observed dipyridamole induced increase in gap junction coupling in endothelial cells is related to a cAMP-PKA dependent phosphorylation pathway. The report shows that gap junction coupling in endothelial cells is a suitable therapeutic target for treatment of cardiovascular diseases.
KW - Animals
KW - Cattle
KW - Cell Line
KW - Connexins/metabolism
KW - Cyclic AMP-Dependent Protein Kinases/antagonists & inhibitors
KW - Dipyridamole/pharmacology
KW - Endothelial Cells/drug effects
KW - Fibrinolytic Agents/pharmacology
KW - Gap Junctions/drug effects
KW - Isoquinolines/pharmacology
KW - Models, Biological
KW - Protein Kinase Inhibitors/pharmacology
KW - Sulfonamides/pharmacology
U2 - 10.1007/s10863-009-9262-2
DO - 10.1007/s10863-009-9262-2
M3 - Article
C2 - 20054624
VL - 42
SP - 79
EP - 84
JO - Journal of Bioenergetics and Biomembranes
JF - Journal of Bioenergetics and Biomembranes
SN - 0145-479X
IS - 1
ER -