Effect of the protein kinase C inhibitor GF 109 203X on elastase release and respiratory burst of human neutrophils |
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| Affiliation: | 1. School of Earth and Environmental Sciences, The University of Queensland, Brisbane, Queensland 4072, Australia;2. School of Business, The University of Queensland, Brisbane, Queensland 4072, Australia;1. Molecular Toxicology Unit, Institute for Medical Research and Occupational Health, Croatia;2. Croatian Institute for Brain Research & Department of Physiology, School of Medicine, University of Zagreb, Croatia;3. Croatian Academy of Sciences and Arts (HAZU), Zagreb, Croatia;1. Molecular and Structural Biology Division, CSIR-Central Drug Research Institute, Lucknow, India;2. Cell Biology Lab, National Institute of Immunology, New Delhi, India |
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| Abstract: | - 1.1. The effects of bisindolylmaleimide GF 109 203X, reported to be a potent and highly selective inhibitor of protein kinase C (PKC), have been investigated on some human neutrophil functions.
- 2.2. GF 109 203X prevented O2− production by NADPH-oxidase whatever the stimulus used for polymorphonuclear neutrophil (PMN) activation: directs PKC activators like phorbol myristate acetate (PMA) and dioctanoylglycerol, calcium ionophore (A23187), or receptor agonists like fMet-Leu-Phe (fMLP) and opsonized zymosan.
- 3.3. The effect of GF 109 203X was also examined on elastase exocytosis by neutrophils. PMA-mediated elastase release was prevented by GF 109 203X. However, GF 109 203X had no effect on exocytosis induced by A23187 and the effect of this compound on the fMLP response changed according to its concentration.
- 4.4. These data suggest that PKC might be essential for stimulus-mediated O2− production and also that PKC plays only a minor role in elastase secretion as compared to the role of the cytosolic calcium level.
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