NO regulates LPS-stimulated cyclooxygenase gene expression and activity in pulmonary artery endothelium
| العنوان: | NO regulates LPS-stimulated cyclooxygenase gene expression and activity in pulmonary artery endothelium |
|---|---|
| المؤلفون: | Brian W. Christman, Leonard C. Berry, Barbara Meyrick, Paul R. Myers, Jian-Xiong Chen, Miles A. Tanner |
| المصدر: | American Journal of Physiology-Lung Cellular and Molecular Physiology. 280:L450-L457 |
| بيانات النشر: | American Physiological Society, 2001. |
| سنة النشر: | 2001 |
| مصطلحات موضوعية: | Lipopolysaccharides, Pulmonary and Respiratory Medicine, Time Factors, Endothelium, Physiology, Gene Expression, Prostaglandin, Pulmonary Artery, Biology, Pharmacology, Nitric Oxide, Nitric oxide, chemistry.chemical_compound, Physiology (medical), medicine.artery, medicine, Animals, Nitric Oxide Donors, Cyclic GMP, Cells, Cultured, Cell Biology, Isoenzymes, Endothelial stem cell, medicine.anatomical_structure, Eicosanoid, chemistry, Cyclooxygenase 2, Prostaglandin-Endoperoxide Synthases, Immunology, Pulmonary artery, Cyclooxygenase 1, Prostaglandins, biology.protein, Cattle, Endothelium, Vascular, Cyclooxygenase, Blood vessel |
| الوصف: | We examined whether nitric oxide (NO) inhibits prostanoid synthesis through actions on cyclooxygenase (COX) gene expression and activity. Bovine pulmonary artery endothelial cells were pretreated for 30 min with the NO donors 1 mM S-nitroso- N-acetylpenicillamine (SNAP), 0.5 mM sodium nitroprusside (SNP), or 0.2 μM spermine NONOate; controls included cells pretreated with either 1 mM N-acetyl-d-penicillamine or the NO synthase (NOS) inhibitor 1 mM N G-nitro-l-arginine methyl ester with and without addition of lipopolysaccharide (LPS; 0.1 μg/ml) for 8 h. COX-1 and COX-2 gene and protein expression were examined by RT-PCR and Western analysis, respectively; prostanoid measurements were made by gas chromatography-mass spectrometry, and COX activity was studied after a 30-min incubation with 30 μM arachidonic acid. LPS induced COX-2 gene and protein expression and caused an increase in COX activity and an eightfold increase in 6-keto-PGF1αrelease. LPS-stimulated COX-2 gene expression was decreased by ∼50% by the NO donors. In contrast, LPS caused a significant reduction in COX-1 gene expression and treatment with NO donors had little effect. SNAP, SNP, and NONOate significantly suppressed LPS-stimulated COX activity and 6-keto-PGF1α release. Our data indicate that increased generation of NO attenuates LPS-stimulated COX-2 gene expression and activity, whereas inhibition of endogenous NOS has little effect. |
| تدمد: | 1522-1504 1040-0605 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::8016da2aa0abf6a13638851070da43b4Test https://doi.org/10.1152/ajplung.2001.280.3.l450Test |
| رقم الانضمام: | edsair.doi.dedup.....8016da2aa0abf6a13638851070da43b4 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15221504 10400605 |
|---|