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M J Zhou

Publications and source records attributed to M J Zhou.

11 recordsLinked to original sources
PubMed1998

Oscillatory pericellular proteolysis and oxidant deposition during neutrophil locomotion.

To better understand the mechanism of leukocyte migration in complex environments, model extracellular matrices were prepared using gelatin, Hanks' solution, Bodipy-BSA (fluorescent upon proteolysis), and dihydrotetramethylrosamine or hydroethidine (fluorescent upon oxidation). Using quantitative microfluorometry, neutrophil-mediated extracellular pulses of reactive oxygen metabolites (ROMs) and pericellular proteolysis were periodically observed showing that these functions occur as quantal bursts. However, chronic granulomatous disease neutrophils, which do not produce ROMs, did not display ROM deposition. Matrices show an alternating pattern of green (proteolytic) and red (oxidative) fluorescence, indicating these functions are out of phase. Electric fields phase-matched with metabolic oscillations, which increase the amplitude of intracellular NAD(P)H oscillations, increase ROM deposition and pericellular proteolysis; this further supports the link between intracellular chemical oscillators and extracellular functions. This phase relationship may allow ROMs to inactivate protease inhibitors, followed by protease activation.

Adult↗
PubMed1997

A cytosolic calcium transient is not necessary for degranulation or oxidative burst in immune complex-stimulated neutrophils.

Receptor-mediated activation of neutrophils (PMN) initiates possibly interdependent events, including a rapid transient increase in [Ca2+]i, implicated as a second messenger. To investigate whether this transient is required for eventual degranulation, PMN were incubated with an intracellular Ca2+ chelator (BAPTA), then exposed to chemotactic peptide [N-formyl-methionyl-leucyl-phenylalanine (fMLP)l with or without cytochalasin B (CB) or to high-valency immune complexes (HIC); delta[Ca2+]i, delta(pH)i, oxidative burst, and elastase release were then evaluated (plus or minus EGTA 15 s before stimulation) after 2 and 15 min incubation in 0.9 mM Ca2+. With either fMLP plus CB or HIC stimulation, BAPTA-treated cells were unable to achieve a Ca2+ transient with a 2-min incubation, whereas a 15-min incubation allowed the BAPTA-treated cells to recover a portion of the delta[Ca2+]i. Even though BAPTA-treated cells were unable to mount a delta[Ca2+]i at 2 min, HIC-stimulated BAPTA-treated cells were able to elicit an oxidative burst (33% of control) and degranulation (67% of control). Therefore, we conclude that delta[Ca2+]i modulates but is not required for oxidative burst or degranulation.

Antigen-Antibody Complex↗
PubMed1995

Distinct tyrosine kinase activation and Triton X-100 insolubility upon Fc gamma RII or Fc gamma RIIIB ligation in human polymorphonuclear leukocytes. Implications for immune complex activation of the respiratory burst.

Two tyrosine kinase-dependent pathways exist for activation of the respiratory burst by polymorphonuclear leukocyte (PMN) immunoglobulin G Fc receptors. Direct ligation of Fc gamma RII activates the respiratory burst, but ligation of the glycan phosphoinositol-linked Fc gamma RIIIB does not. Instead, this receptor and the integrin complement receptor CR3 synergize in activation of the respiratory burst (Zhou, M.-J., and Brown, E. J. (1994) J. Cell Biol. 125, 1407-1416). Here we show that direct ligation of Fc gamma RII leads to activation and Triton X-100 insolubility of the Src family kinase Fgr, without effect on the related myeloid Src family member Hck. In contrast, adhesion of PMN via Fc gamma RIIIB leads to activation and Triton X-100 insolubility of Hck but not Fgr. The exclusive association of Fc gamma RIIIB with Hck activation and Triton insolubility is not solely a result of its glycan phosphoinositol anchor, since decay accelerating factor (CD55), another prominent glycan phosphoinositol-anchored PMN protein, is associated with Fgr insolubility to a greater extent than Hck. Ligation of decay accelerating factor, with or without coligation of CR3, does not activate the PMN respiratory burst. Coligation of Fc gamma RIIIB with Fc gamma RII overcomes the pertussis toxin inhibition of H2O2 production in response to direct ligation of Fc gamma RII. These data support the hypothesis that activation of Hck upon Fc gamma RIIIB ligation has a role in generation of the synergistic respiratory burst.

Antigen-Antibody Complex↗
PubMed1994

CR3 (Mac-1, alpha M beta 2, CD11b/CD18) and Fc gamma RIII cooperate in generation of a neutrophil respiratory burst: requirement for Fc gamma RIII and tyrosine phosphorylation.

Cooperation among plasma membrane receptors in activating signal transduction cascades is not well understood. For almost 20 years, it has been clear that when a particulate foreign body is opsonized with complement as well as IgG, the efficiency of IgG effector functions is markedly enhanced. However, the molecular mechanisms involved in cooperation between IgG Fc receptors and complement receptors have not been elucidated. In this work, we show that when human neutrophils (PMN) are plated on a surface coated with both anti-CR3 and anti-Fc gamma RIII antibodies, the respiratory burst which occurs is equivalent to that stimulated by anti-Fc gamma RII. The CR3 ligand iC3b is as effective as anti-CR3 for cooperating with anti-Fc gamma RIII in generation of a respiratory burst. The synergy between CR3 and Fc gamma RIII for activating the NADPH oxidase is abolished by Fab of anti-Fc gamma RII. Nonetheless, the observed synergy is not an artifact of unintended Fc gamma RII ligation, since (a) only this combination of antibodies works to generate H2O2; (b) coating plates with either of the antibodies alone cannot activate the respiratory burst at any dose; (c) LAD (CR3 deficient) cells, which are perfectly competent to mount a respiratory burst when Fc gamma RII is engaged, are incapable of activating the respiratory burst when adherent to wells coated with anti-Fc gamma RIII and anti-CR3; (d) direct engagement of Fc gamma RII activates the respiratory burst by a pathway pharmacologically distinguishable from the synergistic respiratory burst. Fc gamma RIII/CR3 synergy is abolished by cytochalasin B and herbimicin, suggesting that both the actin cytoskeleton and tyrosine phosphorylation are necessary for activation of the synergistic respiratory burst. Further analysis shows that CR3 and Fc gamma RIII have distinct roles in activation of this Fc gamma RII-dependent assembly of the NADPH oxidase. Ligation of CR3 is sufficient to lead to Fc gamma RII association with the actin cytoskeleton on the adherent PMN surface. Coligation of Fc gamma RIII is required for tyrosine phosphorylation of Fc gamma RII. These data are consistent with a model in which phosphorylation of Fc gamma RII or a closely associated substrate initiates activation of a signal transduction pathway leading to oxidase assembly. These are the first data to demonstrate a molecular mechanism for synergy between IgG Fc and complement receptors in activation of phagocyte effector functions.

Antibodies, Monoclonal↗
PubMed1993

Superoxide-mediated lysis of erythrocytes: the role of colloid-osmotic forces.

Although superoxide anions are a well-known mediator of cytotoxicity, their mechanism of target cell lysis is not clearly understood. In the present study we have used an exogenous source of superoxide to study erythrocyte cytolysis. RBC lysis was studied in buffers containing the cations Li+, Na+, K+, Rb+, and Cs+; superoxide anions were produced and available in these buffers. During this model superoxide-dependent cytolytic process, erythrocytes underwent a shape change from biconcave disk to sphere as shown by scanning electron microscopy. Soret band transmitted light microscopy has confirmed this shape change and shown that it precedes cytosolic oxidation. This evidence is consistent with a colloid-osmotic type lytic mechanism. Erythrocyte lysis was studied by 51Cr-release and light scattering methods. Superoxide-mediated target cytolysis was characterized by: 1) a sigmoidal dose-response curve and 2) a lag time in cytolysis after superoxide addition in kinetic light scattering experiments. The efficacy of cytolysis followed the rank order Cs+ > Rb+ > Na+, Li+ > sucrose = raffinose, which provides additional support for a colloid-osmotic lytic mechanism. Furthermore, the rank order potency correlates with the cations' hydration numbers. We suggest that oxidative events trigger the formation of colloid-osmotic pores approximately 1 nm in diameter.

Buffers↗
PubMed1992

Surface-bound immune complexes trigger transmembrane proximity between complement receptor type 3 and the neutrophil's cortical microfilaments.

To characterize the transmembrane associations participating in antibody-dependent binding, we have used resonance energy transfer (r.e.t.) microscopy to assess the molecular proximity of complement receptor type 3 (CR3) and Fc gamma R type II (Fc gamma RII) and type III (Fc gamma RIII) with microfilaments during neutrophil adherence to untreated surfaces, surfaces coated with BSA, surfaces coated with BSA/anti-BSA F(ab')2 complexes, or surfaces coated with BSA/anti-BSA rabbit IgG immune complexes. Receptors were labeled with fluorescein-conjugated antireceptor Fab fragments, whereas microfilaments were labeled with rhodamine-phalloidin. CR3-to-microfilament r.e.t. was dramatically increased in neutrophils adherent to IgG immune complex-coated surfaces but not untreated or control surfaces. However, the low level of r.e.t. between donor-labeled anti-Fc gamma RII Fab fragments and rhodamine-phalloidin was not affected by any condition including surface-bound immune complexes. Significant r.e.t. levels between Fc gamma RIII and microfilaments were not found under any condition. We suggest that CR3 plays an important role in tethering surface-attached immune complexes to the neutrophil's cytoskeleton.

Actin Cytoskeleton↗
PubMed1991

Oxidative damage by phenylhydrazine diminishes erythrocyte anion transport.

Human erythrocytes were exposed to oxidative stress by treatment with the slowly hemolytic drug phenylhydrazine. Phenylhydrazine has been previously shown to trigger the production of toxic oxygen metabolites including O-2 and H2O2 and the formation of Heinz bodies. The concentration-dependent formation of Heinz bodies was confirmed using optical microscopy. Heinz body formation was accompanied by surface protuberances as shown by scanning electron microscopy. The formation of Heinz bodies was accompanied by inhibition of anion translocation. Anion translocation was measured using the anionic fluorescent substrate analog N-(2-aminoethylsulfonate)-7-nitrobenz-2-oxa-1,3-diazole (NBD-taurine). The efflux of NBD-taurine was measured by continuous monitoring of transport by fluorescence (CMTF). The mean value of the kinetic rate constant for transport, k, was found to be -0.090 +/- 0.017 min-1. Phenylhydrazine was found to decrease k to less than one-half of control values in a dose-dependent fashion. The disruption of anion translocation may be related to the oxidative effects of phenylhydrazine and to the generation of Heinz bodies, which bind to the N-terminal domain of band 3.

Adult↗
PubMed1991

Detection of transmembrane linkages between immunoglobulin or complement receptors and the neutrophil's cortical microfilaments by resonance energy transfer microscopy.

By exploiting the 1/r4 (where r is the separation distance between fluorochromes) dependence of energy transfer between parallel lamellae, we have observed transmembrane energy transfer between membrane receptors and cortical microfilaments. Receptors were labeled with donor- or acceptor-conjugated Fab fragments, whereas microfilaments were labeled with acceptor- or donor-conjugated phalloidin reagents. Energy transfer was imaged by optical microscopy. We report that cell surface receptors can be constitutively unlinked, linked or inducibly linked to microfilaments.

Actin Cytoskeleton↗
PubMed1986

[Pleomorphic carcinoma of the pancreas--report of 3 cases].

The incidence of pleomorphic carcinoma of the pancreas is low. In 34 cases of non-endocrinic cancer of the pancreas detected pathologically by operation and autopsy in our hospital from 1961 to 1984, 3 were pleomorphic carcinoma, comprising 8.8%. In histology, the tumor was clearly characterized by the bizarre uninuclear and multinuclear giant cells with abundant eosinophilic cytoplasm and malignant spindle cells. In these 3 cases, the tumor was originated from the acinic epithelium in 2 and from the ductal epithelium in 1. This tumor should be differentiated from pleomorphic rhabdomyosarcoma, liposarcoma, fibrosarcoma and lymphosarcoma, etc.

Adult↗
PubMed1985

[Adenoma of the gallbladder--pathologic analysis of 14 cases].

Adenoma of the gallbladder is a rare benign tumor. We found fourteen in 2600 surgical specimens of cholecystectomy, an incidence of 0.55%. Three are male and eleven female Adenoma of the gallbladder is divided into two types: papilloma and tubular. Adenoma of the gallbladder might be a precancerous lesion. We found atypical hyperplasia in four and carcinomatous change in two of these fourteen adenomas. All the patients were complicated by chronic cholecystitis, and twelve by one or several stones. Chronic inflammation and the stone formation might be the etiological factors of adenoma of the gallbladder. In this paper, the histological features and differential diagnosis are discussed. We had also observed the mucinous change of this adenoma, atypical hyperplasia and carcinomatous degeneration by histochemical means.

Adenoma↗