Generation of the neutrophil-activating peptide-2 by cathepsin G and cathepsin G-treated human platelets
| Autor: | E. J. Miller, G. Mullenbach, M. A. L. Atkinson, M. D. Stevens, A. B. Cohen |
|---|---|
| Rok vydání: | 1992 |
| Předmět: |
Blood Platelets
Peptide Biosynthesis Pulmonary and Respiratory Medicine Cathepsin G Neutrophil-Activating Peptide 2 Neutrophils Physiology chemistry.chemical_compound Physiology (medical) Macrophages Alveolar mental disorders Chymotrypsin Humans Medicine Platelet Protease-activated receptor Platelet activation Cells Cultured Pancreatic Elastase biology business.industry musculoskeletal neural and ocular physiology Serine Endopeptidases fungi Cell Biology Neutrophil extracellular traps beta-Thromboglobulin Cathepsins Molecular biology Culture Media chemistry Neutrophil elastase Immunology Neutrophil degranulation biology.protein Leukocyte Elastase Peptides business human activities psychological phenomena and processes |
| Zdroj: | American Journal of Physiology-Lung Cellular and Molecular Physiology. 263:L249-L256 |
| ISSN: | 1522-1504 1040-0605 |
| DOI: | 10.1152/ajplung.1992.263.2.l249 |
| Popis: | The neutrophil-activating peptide-2 (NAP-2) is a cytokine that is generated by the proteolytic cleavage of a precursor protein and that causes neutrophil degranulation and chemotaxis. NAP-2 precursors are produced in platelets and are normally found in the circulation. We showed that NAP-2 is generated by the action of neutrophil cathepsin G on two of the precursors, the connective tissue-activating peptide-III (CTAP-III) and beta-thromboglobulin (beta-TG). However, neutrophil elastase degraded the precursors to inactive peptides. The specific binding of cathepsin G to platelets caused the platelets to secrete NAP-2, and cathepsin G bound to the platelets could still generate NAP-2 from its precursor proteins. In addition, activated neutrophils in the presence of platelets generated NAP-2 from its precursors and caused platelets to secrete NAP-2. These studies demonstrate a unique mechanism for the activation of neutrophils through the interaction of neutrophils, platelets, and NAP-2 precursors that are released either by activated platelets or are present in circulation. It is therefore possible that NAP-2 may be generated at sites where aggregations of neutrophils and platelets occur in vessels such as pulmonary capillaries in patients with the adult respiratory distress syndrome and coronary arteries in patients with evolving myocardial infarctions. |
| Databáze: | OpenAIRE |
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