Effects of endothelin-1 and nitric oxide on proliferation of cultured guinea pig bronchial smooth muscle cells
| Autor: | Hajime Murakami, Yasuo Kizawa, Nozomi Ohuchi, Kiyoshige Saito, Tadashi Kusama |
|---|---|
| Rok vydání: | 2001 |
| Předmět: |
Endothelin Receptor Antagonists
Male medicine.medical_specialty Physiology Health Toxicology and Mutagenesis Guinea Pigs Bronchi Biology Nitric Oxide Toxicology Peptides Cyclic Biochemistry Nitric oxide chemistry.chemical_compound Epidermal growth factor Quinoxalines Internal medicine medicine Animals Enzyme Inhibitors Receptor Cells Cultured Oxadiazoles BQ-123 Endothelin-1 Muscle Smooth Cell Biology General Medicine BQ-788 Endothelin 1 Endocrinology chemistry Guanylate Cyclase Molsidomine Respiratory epithelium Soluble guanylyl cyclase Cell Division |
| Zdroj: | Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology. 128:495-501 |
| ISSN: | 1532-0456 |
| DOI: | 10.1016/s1532-0456(01)00172-7 |
| Popis: | The proliferative effects of endothelin-1 (ET-1), both alone and in combination with epidermal growth factor (EGF), and the effect of nitric oxide (NO) on the cell proliferation were investigated in cultured guinea pig bronchial smooth muscle cells. ET-1 (10-100 nM) alone augmented cell proliferation, and was additive to the effect of EGF (0.48 nM) in a concentration-dependent manner. An ET(A) antagonist, BQ-123 (10 microM), reduced the cell-proliferative effect of ET-1, whereas an ET(B) antagonist, BQ-788 (10 microM), did not influence the effect. A NO donor, SIN-1 (10 nM-1 microM), reduced the cell-proliferative effect of ET-1 in a concentration-dependent manner. The effect of SIN-1 (1 microM) was partly, but significantly, reversed by a soluble guanylyl cyclase inhibitor, ODQ (1 microM). These results suggest that ET-1 acts not only as a co-mitogen with EGF but also as a mitogen alone, and that its action is mediated through activation of ET(A) receptors. Therefore, ET-1 may contribute to airway remodeling, a pathophysiological hallmark of asthma. In addition, NO, which is produced mainly in the airway epithelium and is partly mediated through cGMP-dependent pathway, may reduce the phenomenon. |
| Databáze: | OpenAIRE |
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