Exogenous nitric oxide inhibits shedding of ADAM17 substrates
Autor: | Karolina Wawro, Joanna Bereta, Monika Bzowska, Katarzyna Duda, Renata Mężyk-Kopeć, Krystyna Stalińska, Sudipta Das |
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Rok vydání: | 2009 |
Předmět: |
TNF
Endogeny Inflammation ADAM17 Protein Biology Nitric Oxide General Biochemistry Genetics and Molecular Biology Cell Line Nitric oxide shedding Mice chemistry.chemical_compound nitric oxide medicine Animals Nitric Oxide Donors RNA Messenger Receptor Cell Line Transformed ADAM17 Enzyme Precursors Tumor Necrosis Factor-alpha Macrophages Monocyte Endothelial Cells TNF receptor 1 Flow Cytometry Cell biology Nitric oxide synthase ADAM Proteins Kinetics medicine.anatomical_structure chemistry Ectodomain Biochemistry Receptors Tumor Necrosis Factor Type I Protein Biosynthesis Antigens Surface Metalloproteases biology.protein Tumor necrosis factor alpha medicine.symptom |
Zdroj: | Scopus-Elsevier Europe PubMed Central |
ISSN: | 1734-154X 0001-527X 5839-1584 |
Popis: | Both ADAM17, the secretase responsible for the shedding of ectodomains of numerous membrane proteins including TNF and its receptors, as well as nitric oxide synthesized by inducible nitric oxide synthase play regulatory roles in inflammation and tumor progression. We analyzed the effect of endogenous and exogenous nitric oxide on the expression and activity of ADAM17 in murine endothelial cells and a monocyte/macrophage cell line. We found that endogenous nitric oxide influenced neither ADAM17 mRNA level nor the shedding of two ADAM17 substrates, TNF and TNFR1. Exogenous NO significantly diminished the release of TNF and TNFR1 without affecting the ADAM17 transcript level. Our data seem contrary to a previous report that showed the activation of ADAM17 by nitric oxide (Zhang et al., 2000, J Biol Chem 275: 15839-15844). We discuss potential mechanisms of NO-mediated inhibition of ectodomain shedding and possible reasons of discrepancy between our results and the previous report. |
Databáze: | OpenAIRE |
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