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Nitric Oxide Regulates the Aggregation of Stimulated Human Neutrophils
Linköping University, Department of Molecular and Clinical Medicine, Medical Microbiology. Linköping University, Faculty of Health Sciences.
Linköping University, Department of Molecular and Clinical Medicine, Medical Microbiology. Linköping University, Faculty of Health Sciences.
Linköping University, Department of Molecular and Clinical Medicine, Medical Microbiology. Linköping University, Faculty of Health Sciences.
2000 (English)In: Biochemical and Biophysical Research Communications - BBRC, ISSN 0006-291X, E-ISSN 1090-2104, Vol. 274, no 2, 482-487 p.Article in journal (Refereed) Published
Abstract [en]

Neutrophil aggregation is mediated by both CD18 integrin and L-selectin. Nitric oxide attenuates the integrin-mediated adhesion of neutrophils to collagen and to endothelium and may therefore affect aggregation as well. FMLP-stimulated neutrophils exposed to -arginine showed increased and prolonged aggregation, whereas cells pretreated with L-NAME did not differ from FMLP-stimulated controls. Nitric oxide is known to induce ADP ribosylation of G-actin, which inhibits polymerization. We detected equivalent levels of total F-actin in cells pretreated with -arginine or L-NAME and non-pretreated controls. However, neutrophils pretreated with -arginine and stimulated by CD18 integrin cross-linking exhibited a more limited increase in total F-actin, compared to control and L-NAME-pretreated cells. Thus at least two signaling pathways may be involved FMLP-stimulated aggregation, mediated by CD18 integrins. More specifically, it is plausible that FMLP-receptor signaling upregulates CD18 integrins and endogenous NO subsequently modulates CD18-mediated signaling to prolong aggregation, possibly through ADP-ribosylation of actin.

Place, publisher, year, edition, pages
2000. Vol. 274, no 2, 482-487 p.
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:liu:diva-25912DOI: 10.1006/bbrc.2000.3156Local ID: 10354OAI: oai:DiVA.org:liu-25912DiVA: diva2:246460
Available from: 2009-10-08 Created: 2009-10-08 Last updated: 2017-12-13Bibliographically approved
In thesis
1. The role of nitric oxide in cytoskeleton-mediated organelle transport and cell adhesion
Open this publication in new window or tab >>The role of nitric oxide in cytoskeleton-mediated organelle transport and cell adhesion
2001 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Nitric oxide (NO) is a signaling molecule that is produced by many different kinds of cells, and it is known to mediate actions such as blood vessel dilation, communication between nerve cells, and killing of bacteria in infections. The cytoskeleton is involved in many important cellular functions, among them intracellular transport of organelles, migration, and cell division. The aim of the present studies was to examine the effects of NO on some of the indicated functions. Homotypic adhesion of human neutrophils, which is mediated by ß2 integrins, is an early step in the inflammatory process. Addition of L-argiriine (the substrate of NO production) to fMLP-stimulated neutrophils increased and prolonged aggregation of the cells. Stimulation of L-arginine-pretreated neutrophils by cross-linking of ß2 integrins attenuated the increase in F-actin, as compared to control cells. These results suggest that the aggregation is prolonged by activation of ß2 integrins and endogenous NO production, two events that together seem to inhibit actin polymerization, possibly via ADP ribosylation.

The effect of NO on intracellular translocation of organelles along the cytoskeleton was studied in Xenopus laevis pigment cells. Inhibition of NO production induced by the drug L-NAME was found to inhibit aggregation of the pigment organelles (melanosomes) and to induce dispersion. Activation of PKC, MEK, and ERKl, but not PKA, was associated with the dispersion, thus NO may negatively regulate these kinases, which, when activated, would induce movement of melanosomes. During melanosome aggregation, the cell center increases in height by approximately 30%. Experiments were performed to determine whether the cell membrane is pushed upwards by actin polymerization and water influx through HgCl2-sensitive aquaporins. The results gave no evidence that either two of these mechanisms affects the upward movement. However, L-NAME caused dispersion and a decrease in cell height, thus NO may play a role in maintaining an aggregated, elevated state. In conclusion, many factors regulate both homotypic aggregation and intracellular organelle transport, and NO seems to prolong homotypic aggregation of neutrophils and regulate melanosome transport by inhibiting PKC, MEK and ERKl.

Place, publisher, year, edition, pages
Linköping: Linköpings universitet, 2001. 48 p.
Series
Linköping University Medical Dissertations, ISSN 0345-0082 ; 660
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-28614 (URN)13769 (Local ID)91-7219-761-7 (ISBN)13769 (Archive number)13769 (OAI)
Public defence
2001-03-02, Elsa Brändströmssalen, Universitetssjukhuset, Linköping, 09:00 (Swedish)
Opponent
Available from: 2009-10-09 Created: 2009-10-09 Last updated: 2015-09-18Bibliographically approved

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Forslund, TonyNilsson, HarrietSundqvist, Tommy

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