LPS induces inflammatory responses in human aortic vascular smooth muscle cells via Toll-like receptor 4 expression and nitric oxide production
| Autor: | Eui-Kyu Noh, Sun-Dong Park, Sook-Kyoung Heo, Won-Hwan Park, Hyun-Jeong Yun |
|---|---|
| Rok vydání: | 2008 |
| Předmět: |
Lipopolysaccharides
Vascular Endothelial Growth Factor A medicine.medical_specialty Vascular smooth muscle Lipopolysaccharide Myocytes Smooth Muscle Immunology Vascular Cell Adhesion Molecule-1 Inflammation Pharmacology Nitric Oxide Cell Line Nitric oxide Proinflammatory cytokine chemistry.chemical_compound Internal medicine medicine Humans Immunology and Allergy Enzyme Inhibitors Aorta biology Interleukin-8 Antibodies Monoclonal Intercellular Adhesion Molecule-1 Toll-Like Receptor 4 Nitric oxide synthase Vascular endothelial growth factor NG-Nitroarginine Methyl Ester Endocrinology Gene Expression Regulation chemistry TLR4 biology.protein lipids (amino acids peptides and proteins) Nitric Oxide Synthase medicine.symptom |
| Zdroj: | Immunology Letters. 120:57-64 |
| ISSN: | 0165-2478 |
| Popis: | Inflammation is an important event in the development of vascular diseases such as hypertension, atherosclerosis, and restenosis. In addition, the stimulation of Toll-like receptor 4 (TLR4) by lipopolysaccharide (LPS) induces the release of critical proinflammatory cytokines that activate potent immune responses. In this study, LPS was found to induce TLR4 expression and increased nitric oxide (NO) production by increasing the expression of inducible nitric oxide synthase (iNOS). Furthermore, LPS was found to induce interleukin (IL)-8 and vascular endothelial growth factor (VEGF) production, as well as intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression. Taken together, these results indicate that LPS induces inflammatory responses in HASMC. Moreover, NOS inhibitor (L-NAME) and anti-TLR 4 mAb reduced the LPS-induced NO, IL-8 and VEGF production and ICAM-1 expression. Additionally, TLR4 expression was reduced by NOS inhibitor. Taken together, these results indicate that LPS-induced inflammatory responses are regulated by TLR4 expression and NO production. |
| Databáze: | OpenAIRE |
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