Volume-dependent regulation of the respiratory burst of activated human neutrophils

Kuchkina, N. V.; Orlov, Sergei N.; Pokudin, N. I.; Чучалин, А. Г.

doi:10.1007/bf02125647

Cited by 20 publications

(9 citation statements)

References 11 publications

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“…Hypertonicity has been previously shown to interfere with several neutrophil functions including superoxide production (26), phagocytosis (27), adhesion, and transmigration (23,28). In addition to these inhibitory effects on neutrophil function, the present studies show that shrinkage actively promotes the premature loss of an important surface adhesion molecule.…”

Section: Figsupporting

confidence: 59%

Cell Volume-dependent Regulation of L-selectin Shedding in Neutrophils

Rizoli

Rotstein

Kapùs

1999

Journal of Biological Chemistry

105

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Neutrophil-mediated organ damage is a common feature of many disease states. We previously demonstrated that resuscitation with hypertonic salt solutions prevented the endotoxin-induced leukosequestration and consequent lung injury, and this effect was partially attributed to an altered surface expression of adhesion molecules, CD11b and L-selectin. In this study we investigated the mechanisms whereby osmotic stress evokes L-selectin shedding. The metalloprotease inhibitor RO 31-9790 prevented the osmotic down-regulation of L-selectin, indicating that this process was catalyzed by the same "sheddase" responsible for L-selectin cleavage induced by diverse inflammatory stimuli. The trigger for hypertonic shedding was cell shrinkage and not increased osmolarity, ionic strength, or intracellular pH. Volume reduction caused robust tyrosine phosphorylation and its inhibition by genistein and erbstatin abrogated shedding. Shrinkage stimulated tyrosine kinases Hck, Syk, and Pyk2, but prevention of their activation by the Src-family inhibitor PP1 failed to affect the Lselectin response. Hypertonicity elicited the Src familyindependent activation of p38, and the inhibition of this kinase by SB203580 strongly reduced shedding. p38 was also essential for the N-formyl-methionyl-leucyl-phenylalanine-and lipopolysaccharide-induced shedding but not the phorbol ester-induced shedding. Thus, cell volume regulates L-selectin surface expression in a p38-mediated, metalloprotease-dependent manner. Moreover, p38 has a central role in shedding induced by many inflammatory mediators.

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Section: Figsupporting

confidence: 59%

Cell Volume-dependent Regulation of L-selectin Shedding in Neutrophils

Rizoli

Rotstein

Kapùs

1999

Journal of Biological Chemistry

105

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“…A reduced flux of glucose through the pentose phosphate shunt decreases the generation of NADPH which is required by the NADPH oxidase for O 2 -formation [129]. Along these lines, osmotic cell shrinkage has been shown to inhibit the oxidative burst in leukocytes [132]. Other mechanisms conceivably contributing to the protective effect of cell shrinkage may be accumulation of stabilizing cellular osmolytes [133], inhibition of the volume regulatory tyrosine kinase Lck 56 [134] and activation of volume regulatory Na + /H + exchanger with subsequent alkalinization.…”

Section: Significance Of Cell Volume In Cell Proliferation and Apoptomentioning

confidence: 99%

Cell Volume in the Regulation of Cell Proliferation and Apoptotic Cell Death

Läng¹,

Ritter²,

Gamper³

et al. 2000

Cell Physiol Biochem

227

181

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Cell proliferation must – at some time point – lead to increase of cell volume and one of the hallmarks of apoptosis is cell shrinkage. At constant extracellular osmolarity those alterations of cell volume must reflect respective changes of cellular osmolarity which are hardly possible without the participation of cell volume regulatory mechanisms. Indeed, as shown for ras oncogene expressing 3T3 fibroblasts, cell proliferation is paralleled by activation of Na⁺/H⁺ exchange and Na⁺,K⁺,2Cl^- cotransport, the major transport systems accomplishing regulatory cell volume increase. Conversely, as evident from CD95-induced apoptotic cell death, apoptosis is paralleled by inhibition of Na⁺/H⁺ exchanger and by activation of Cl^- channels and release of the organic osmolyte taurine, major components of regulatory cell volume decrease. However, ras oncogene activation leads to activation and CD95 receptor triggering to inhibition of K⁺ channels. The effects counteract the respective cell volume changes. Presumably, they serve to regulate cell membrane potential, which is decisive for Ca⁺⁺ entry through I_CRAC and the generation of cytosolic Ca⁺⁺ oscillations in proliferating cells. As a matter of fact I_CRAC is activated in ras oncogene expressing cells and inhibited in CD95-triggered cells. Activation of K⁺ channels and Na⁺/H⁺ exchanger as well as Ca⁺⁺ oscillations have been observed in a wide variety of cells upon exposure to diverse mitogenic factors. Conversely, diverse apoptotic factors have been shown to activate Cl^- channels and organic osmolyte release. Inhibition of K⁺ channels is apparently, however, not a constant phenomenon paralleling apoptosis which in some cells may even require the operation of K⁺ channels. Moreover, cell proliferation may at some point require activation of Cl^- channels. In any case, the alterations of cell volume are obviously important for the outcome, as cell shrinkage impedes cell proliferation and apoptosis can be elicited by increase of extracellular osmolarity. At this stage little is known about the interplay of cell volume regulatory mechanisms and the cellular machinery leading to mitosis or death of the cell. Thus, considerable further experimental effort is required in this exciting area of cell physiology.

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“…It should be stressed, however, that the impact of cell-volume perturbations on cellular physiology is not exclusively negative. Thus cell volume serves as a physiological modulator of cellular functions in hepatocytes, epithelial cells, brain glial cells, and a variety of migrating cells (20,21,(23)(24)(25)29). In the kidneys, the transepithelial transport of electrolytes across the basolateral and apical membranes of secretory cells is thought to be coordinated by changes in cellular volume that strongly regulate the activity of volume-sensitive K ϩ and Cl Ϫ channels as well as ion carriers, including the Na…”

mentioning

confidence: 99%