Mobilization of sialidase from intracellular stores to the surface of human neutrophils and its role in stimulated adhesion responses of these cells.

Cross, Alan S.; Wright, Daniel G.

doi:10.1172/jci115536

Cited by 91 publications

(93 citation statements)

References 60 publications

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“…This finding is consistent with the observation of Hart et al 23 They found reduced binding of the sialic acid-specific lectins derived from Limulus polyphemus Maackia amurensis (MAL II), and Sambucus nigra to surfaces of apoptotic neutrophils when compared with viable cells. However, they did not observe an increased binding of the galactose recognizing lectin peanut agglutinin implying that complete desialylation caused by activated sialidases 24 did not represent a major carbohydrate modification event accompanying apoptosis. We observed that reduced binding of MAL I preceded cell shrinkage suggesting that very early membrane changes result in a partial loss of sialic acid.…”

Section: Calnexin and Er-tracker Co-localize Intracellular In Permeabmentioning

confidence: 91%

After shrinkage apoptotic cells expose internal membrane-derived epitopes on their plasma membranes

et al. 2006

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Apoptosis and phagocytosis of apoptotic cells are crucial processes. At best the phagocytic machinery detects and swallows all apoptotic cells in a way that progression to secondary necrosis is avoided. Otherwise, inflammation and autoimmune diseases may occur. Most apoptotic cells are phagocytosed instantaneously in a silent fashion; however, some dying cells escape their clearance. If the cells are not cleared early, they lose membranes due to extensive shedding of membrane surrounded vesicles (blebbing) and shrink. It is unclear how apoptotic cells compensate their massive loss of plasma membrane. Here, we demonstrate that endoplasmic reticulum-(ER) resident proteins (calnexin, the KDEL receptor and a dysfunctional immunoglobulin heavy chain) were exposed at the surfaces of shrunken late apoptotic cells. Additionally, these cells showed an increased binding of lectins, which recognize sugar structures predominantly found as moieties of incompletely processed proteins in ER and Golgi. In addition the ER resident lipophilic ER-Trackert Blue-White DPX, and internal GM1 were observed to translocate to the cell surfaces during late apoptosis. We conclude that during blebbing of apoptotic cells the surface membrane loss is substituted by immature membranes from internal stores. This mechanism explains the simultaneous appearance of preformed recognition structures for several adaptor proteins known to be involved in clearance of dead cells.

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Section: Calnexin and Er-tracker Co-localize Intracellular In Permeabmentioning

confidence: 91%

After shrinkage apoptotic cells expose internal membrane-derived epitopes on their plasma membranes

et al. 2006

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“…Endogenous neuraminidase activity may give rise to desialation of neutrophil surface carbohydrates following agonist induced activation. 26 However, the carbohydrate moieties examined here are differentially regulated following fMLP stimulation: expression of CD15 is augmented, CDw65 shows little change, and there is marked downregulation of CDw17. 27 In contrast, expression of the surface carbohydrates CDw17 and CDw65 was reduced by 40 ± 50% during neutrophil apoptosis.…”

Section: Neutrophil Surface Carbohydratesmentioning

confidence: 68%

Molecular characterization of the surface of apoptotic neutrophils: Implications for functional downregulation and recognition by phagocytes

et al. 2000

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We have used a panel of monoclonal antibodies and lectins to examine the profile of surface molecule expression on human neutrophils that have undergone spontaneous apoptosis during in vitro culture. Neutrophil apoptosis was found to be accompanied by down-regulation of the immunoglobulin superfamily members PECAM-1 (CD31), ICAM-3 (CD50), CD66acde, and CD66b and the integrin-associated proteins CD63 and urokinase plasminogen activator receptor (CD87) that may alter the potential for adhesive interactions. Cellular interactions may be further influenced by the reduction of the expression of surface carbohydrate moieties, including sialic acid. Reduced expression of FcgRII (CD32), complement receptor type 1 (CD35) and receptors for pro-inflammatory mediators C5a (CD88) and TNFa (CD120b) associated with apoptosis might limit neutrophil responsiveness to stimuli that trigger degranulation responses. Although many of the receptors we have examined are expressed at reduced levels on apoptotic neutrophils, we found that there was differential loss of certain receptors (e.g. CD16, CD15 and CD120b) and increased expression of aminopeptidase-N (CD13). Together with our previous data showing that expression of certain molecules e.g. LFA-3 (CD58) is not altered during neutrophil apoptosis, these data are suggestive of specific changes in receptor mobilisation and shedding associated with apoptosis. Although reduced expression of CD63 (azurophilic granules) and CR1 (specific granules) indicates that granule mobilisation does not accompany apoptosis, a monoclonal antibody (BOB78), that recognises a 90 kDa antigen localised in intracellular granules, defines a subpopulation of apoptotic neutrophils that exhibit nuclear degradation yet retain intact plasma membranes. BOB78 positive neutrophils were found to bind biotinylated thrombospondin, suggesting that this mAb defines surface molecular changes associated with exposure of thrombospondin binding moieties. Cell Death and Differentiation (2000) 7, 493 ± 503.

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“…Sialidase is overexpressed during the activation of T cells, B cells, macrophages, and neutrophils [Landolfi et al, 1985;Landolfi and Cook, 1986;Cross and Wright, 1991] (N. Stamatos, private communication). The induced enzyme is targeted to the plasma membrane and is responsible for processing different molecules expressed on the cell surface, resulting in their hyposialylation [Chen et al, 1997].…”

Section: Future Prospectsmentioning

confidence: 99%

Molecular pathology of NEU1 gene in sialidosis

Poupětová²,

et al. 2003

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Communicated by Mark H. PaalmanLysosomal sialidase (EC 3.2.1.18) has a dual physiological function; it participates in intralysosomal catabolism of sialylated glycoconjugates and is involved in cellular immune response. Mutations in the sialidase gene NEU1, located on chromosome 6p21.3, result in autosomal recessive disorder, sialidosis, which is characterized by the progressive lysosomal storage of sialylated glycopeptides and oligosaccharides. Sialidosis type I is a milder, late-onset, normosomatic form of the disorder. Type I patients develop visual defects, myoclonus syndrome, cherry-red macular spots, ataxia, hyperreflexia, and seizures. The severe early-onset form, sialidosis type II, is also associated with dysostosis multiplex, Hurler-like phenotype, mental retardation, and hepatosplenomegaly. We summarize information on the 34 unique mutations determined so far in the sialidase gene, including four novel missense and one novel nonsense mutations found in two Czech and two French sialidosis patients. The analysis of sialidase mutations in sialidosis revealed considerable molecular heterogeneity, reflecting the diversity of clinical phenotypes that make molecular diagnosis difficult. The majority of sialidosis patients have had missense mutations, many of which have been expressed; their effects on activity, stability, intracellular localization, and supramolecular organization of sialidase were studied. A structural model of sialidase allowed us to localize mutations in the sialidase molecule and to predict their impact on the tertiary structure and biochemical properties of the enzyme. Hum Mutat 22:343-352,

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Mobilization of sialidase from intracellular stores to the surface of human neutrophils and its role in stimulated adhesion responses of these cells.

Cited by 91 publications

References 60 publications

After shrinkage apoptotic cells expose internal membrane-derived epitopes on their plasma membranes

After shrinkage apoptotic cells expose internal membrane-derived epitopes on their plasma membranes

Molecular characterization of the surface of apoptotic neutrophils: Implications for functional downregulation and recognition by phagocytes

Molecular pathology of NEU1 gene in sialidosis

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