Journal
ENDOTHELIUM-JOURNAL OF ENDOTHELIAL CELL RESEARCH
Volume 10, Issue 6, Pages 309-317Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/10623320390272307
Keywords
calcium; cGMP-dependent protein kinases; cytoskeleton; pulmonary edema
Categories
Funding
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [K08HL002933, R01HL067189, R01HL068062] Funding Source: NIH RePORTER
- NHLBI NIH HHS [HL-67189, HL-02933, HL-68062] Funding Source: Medline
Ask authors/readers for more resources
The authors determined the effect of cyclic guanosine 3',5'-monophosphate (cGMP) on hydrogen peroxide (H2O2)-induced barrier dysfunction in bovine lung microvascular endothelial cell (BLMVEC) monolayers and compared the results to bovine pulmonary artery endothelial cells (BPAECs). In BLMVECs, H2O2 (250 muM) 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 ([Ca2+](i)). The cGMP analogue 8-(p-chlorophenylthio)cGMP (8p-CPT-cGMP; 30 or 50 muM) prevented the H2O2-induced decrease in TER (p < .001) as well as the cytoskeletal rearrangement and intercellular gap formation. 8-pCPT-cGMP (50 muM) attenuated the peak (418.8 +/- 42.1 versus 665.2 +/- 38.0 nmol/L; p < .001) and eliminated the sustained increase in [Ca2+], (193.5 +/- 21.3 versus 418.8 +/- 42.1 nmol/L; p < .001) caused by H2O2. 8-pCPT-cGMP also increased TER (14.2% +/- 2.2%; p < .05) and decreased [Ca2+](i) (201.2 +/- 12.5 vs. 214.4 +/- 12.1 nmol/L; p < .03) before H2O2- In BPAECs, 8p-CPT-cGMP significantly attenuated H2O2-induced increases in permeability and [Ca2+](i) but less effectively than in BLMVECs. These results suggest that in BLMVECs, cGMP countered the adverse effects of H2O2 on barrier function by preventing actin cytoskeletal rearrangement and attenuating the increase in [Ca2+](i).
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available