Rapid changes in light scattering from human polymorphonuclear leukocytes exposed to chemoattractants. Discrete responses correlated with chemotactic and secretory functions.

Yuli, I; Snyderman, Ralph

doi:10.1172/jci111345

Cited by 64 publications

(35 citation statements)

References 41 publications

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“…Furthermore, treatment of PMNs with 15(5)-HETE also reduced the PMN right angle light scatter response induced by LTB4 (Fig. 3), another index of cytoskeletal rearrangement (30,31). Several lines of evidence suggested that esterified 15(S)-HETE also blocked PMN transmigration by inhibiting PMN-endothelial cell adhesion mediated by interactions ofCD 11/ CD 1 8 integrins with endothelial cell ligands.…”

Section: Discussionmentioning

confidence: 86%

Remodeling of neutrophil phospholipids with 15(S)-hydroxyeicosatetraenoic acid inhibits leukotriene B4-induced neutrophil migration across endothelium.

Takata¹,

Matsubara²,

Allen³

et al. 1994

J. Clin. Invest.

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Section: Discussionmentioning

confidence: 86%

Remodeling of neutrophil phospholipids with 15(S)-hydroxyeicosatetraenoic acid inhibits leukotriene B4-induced neutrophil migration across endothelium.

Takata¹,

Matsubara²,

Allen³

et al. 1994

J. Clin. Invest.

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“…In addition, a biphasic light scatter response of uncertain origin has been described (38). The first phase of this response has been shown to be Ca" independent (31).…”

mentioning

confidence: 99%

Relationship of actin polymerization and depolymerization to light scattering in human neutrophils: dependence on receptor occupancy and intracellular Ca++.

Sklar¹,

Omann²,

Painter³

1985

The Journal of Cell Biology

173

110

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When exposed to the N-formylated chemoattractant peptides, neutrophils undergo a transient ruffling followed by a polarization that involves a redistribution of F-actin (Fechheimer, M., and S. H. Zigmond, 1983, Cell Motil., 3:349-361). The cells also undergo a biphasic right angle light scatter response whose first phase is maximal 10-15 s after exposure to the stimulus, and whose second phase is longer in duration and maximal only after 1 min or more (Yuli, I., and R. Snyderman, 1984, J. Clin. Invest. 73:1408-1417). We now report that the first phase is accompanied by a transient polymerization of actin (monitored by cytometric analysis of phallacidin staining according to the method of Howard, T. H., and W. H. Meyer, 1984, J. Cell Biol., 98:1265-1271) and the second phase is accompanied by a more sustained polymerization of actin. Based on correlated measurements of ligand binding (Sklar, L. A., D. A. Finney, Z. G. Oades, A. J. Jesaitis, R. G. Painter, and C. G. Cochrane, 1984, J. Biol. Chem., 259:5661-5669) and intracellular Ca++ elevation (under conditions where we use the fluorescent Ca++ chelator Quin 2 to modulate intracellular Ca++ levels), we conclude that this first phase requires less than 100 receptors/cell (out of 50,000) and does not require the release of intracellular stores of Ca++. In contrast, the sustained polymerization requires both the occupancy of thousands of receptors (an estimated 10% of the receptors per minute) and may be somewhat sensitive to the availability of intracellular Ca++. When ligand binding is interrupted, F-actin rapidly depolymerizes with a half-time of no greater than approximately 15 s, and the transient light scatter response decays toward its initial value in parallel. Partial disaggregation of the cells follows the recovery of these responses. Based on these observations, we suggest that transient actin polymerization and transient cell ruffling give rise to transient aggregation as long as degranulation is limited.

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“…Agonist-induced changes in light scattering by suspended leutrophils reflect, in part, the generation of thin, veil-like amellipods [8,10,22]. In contrast to morphological alterations n suspension, neutrophil migration over a substrate depends Fig.…”

Section: Actin Polymerization and Shape Changesmentioning

confidence: 99%

ADP‐ribosylation of Rho enhances actin polymerization‐coupled shape oscillations in human neutrophils

et al. 1995

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Stimulated neutrophils exhibit coordinated sinusoidal oscillations in filamentous actin content and cellular shape. We investigated the effect of inhibition of the small G protein Rho on neutrophil actin polymerization, shape changes and oscillations using a genetically engineered toxin that enters cells and selectively ADP-ribosylates endogenous Rho. This treatment increased the amplitudes and frequencies of shape oscillations and duration of the oscillating transient. However, it had no effect on the initial actin polymerization and shape changes induced by N-formyl-Met-Len-Phe. Regulation of these oscillations may be important for the control of neutrophil motility.

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Rapid changes in light scattering from human polymorphonuclear leukocytes exposed to chemoattractants. Discrete responses correlated with chemotactic and secretory functions.

Cited by 64 publications

References 41 publications

Remodeling of neutrophil phospholipids with 15(S)-hydroxyeicosatetraenoic acid inhibits leukotriene B4-induced neutrophil migration across endothelium.

Remodeling of neutrophil phospholipids with 15(S)-hydroxyeicosatetraenoic acid inhibits leukotriene B4-induced neutrophil migration across endothelium.

Relationship of actin polymerization and depolymerization to light scattering in human neutrophils: dependence on receptor occupancy and intracellular Ca++.

ADP‐ribosylation of Rho enhances actin polymerization‐coupled shape oscillations in human neutrophils

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