| Autor: |
Pearse, David B., Shimoda, Larissa A., Verin, Alexander D., Bogatcheva, Natalia, Moon, Cheit, Ronnett, Gabriete V., Welsh, Laura E., Becker, Patrice M. |
| Předmět: |
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| Zdroj: |
Endothelium; Nov2003, Vol. 10 Issue 6, p309-317, 9p |
| Abstrakt: |
The authors determined the effect of cyclic guanosine 3′,5′-monophosphate (cGMP) on hydrogen peroxide (H 2 O 2 )-induced barrier dysfunction in bovine lung microvascular endothelial cell (BLMVEC) monolayers and compared the results to bovine pulmonary artery endothelial cells (BPAECs). In BLMVECs, H 2 O 2 (250 μM) caused a 31.9% ± 4.8% decrease in transendothelial electrical resistance (TER) associated with increased actin stress fiber formation, intercellular gaps, and intracellular calcium concentration ([Ca 2+ ] i ). The cGMP analogue 8-( p -chlorophenylthio)-cGMP (8p-CPT-cGMP; 30 or 50 μM) prevented the H 2 O 2 -induced decrease in TER ( p < .001) as well as the cytoskeletal rearrangement and intercellular gap formation. 8-pCPT-cGMP (50 μM) attenuated the peak (418.8 ± 42.1 versus 665.2 ± 38.0 nmol/L; p < .001) and eliminated the sustained increase in [Ca 2+ ] i (193.5 ± 21.3 versus 418.8 ± 42.1 nmol/L; p < .001) caused by H 2 O 2 . 8-pCPT-cGMP also increased TER (14.2% ± 2.2%; p < .05) and decreased [Ca 2+ ] i (201.2 ± 12.5 vs. 214.4 ± 12.1 nmol/L; p < .03) before H 2 O 2 . In BPAECs, 8p-CPT-cGMP significantly attenuated H 2 O 2 -induced increases in permeability and [Ca 2+ ] i but less effectively than in BLMVECs. These results suggest that in BLMVECs, cGMP countered the adverse effects of H 2 O 2 on barrier function by preventing actin cytoskeletal rearrangement and attenuating the increase in [Ca 2+ ] i . [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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