Sensitivity of L132 Cells to Some “New” Respiratory Viruses

Bradburne, A. F.

doi:10.1038/221085a0

Cited by 24 publications

(18 citation statements)

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“…The human embryonic lung cell line L132 (10) has been shown to be an excellent tool for cytotoxic tests (11) and for the study of radiation-induced injury (12). In the present study we investigated the effects of glyoxal on lung epithelial cells L132 with particular emphasis on the cytotoxic (apoptotic) effects of glyoxal.…”

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confidence: 98%

Induction of Apoptosis by Glyoxal in Human Embryonic Lung Epithelial Cell Line L132

Kasper

Roehlecke

Witt

et al. 2000

Am J Respir Cell Mol Biol

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Oxidative stress has been suggested to play a central role in the pathogenesis of lung fibrosis and lung epithelial cell apoptosis is considered to be a key event during fibrogenesis. Studies from various laboratories have indicated that metabolic conditions may initiate oxidative stress, thereby contributing to epithelial cell death. This study was designed to test the hypothesis that glyoxal, an intermediate product in the glycation reaction leading to advanced glycation end products (AGEs), may induce lung epithelial cell apoptosis. We investigated the in vitro effects of glyoxal on fetal human lung epithelial L132 cells. Immunocytochemical analysis of paraffin-embedded cells and fluorescence-activated cell sorter analysis revealed a dose-dependent accumulation of the glycoxidation product (epsilon)N-carboxymethyllysine (CML) in all compartments of the cell. It has been shown that CML modification of proteins may serve as an indicator for oxidative stress. To examine the role of apoptosis in epithelial lung cells we investigated glyoxal-dependent changes in pro- and antiapoptotic mediators bax and activated caspase-3, and galectin-3 and bcl-2, respectively. Increasing concentrations of glyoxal (50 to 400 microM) induced an increase in the number of apoptotic cells. The apoptotic changes were confirmed by transmission electron microscopy. Immunocytochemical analysis of treated cells revealed the presence of other AGEs such as pentosidine as well as products of lipid peroxidation.

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confidence: 98%

Induction of Apoptosis by Glyoxal in Human Embryonic Lung Epithelial Cell Line L132

Kasper

Roehlecke

Witt

et al. 2000

Am J Respir Cell Mol Biol

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“…The human embryonic lung epithelial cell line L132 has been shown to be an excellent tool for the study of cytotoxicity (Bradburne 1969;Hildebrand et al 1990;Kasper et al 1999). In a previous study we introduced a model of glyoxal-induced apoptosis in L132 cells (Kasper et al 2000) and we found a dose-dependent accumulation of intracellular CML modifications of cytoplasmic, nuclear and plasma membrane proteins.…”

Section: Introductionmentioning

confidence: 80%

Resistance of L132 lung cell clusters to glyoxal-induced apoptosis

Roehlecke

Kuhnt

Fehrenbach

et al. 2000

Histochem Cell Biol

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Glyoxal is a highly reactive glycating agent involved in the formation of advanced glycation end products (AGEs) and known to induce apoptosis. AGEmediated apoptosis may be an important mechanism of alveolar epithelial remodelling in pulmonary fibrosis. In this study, we investigated the cytotoxic effect of glyoxal on the fetal human epithelial lung cell line L132 under serum-free conditions. This type of culture, which forces the cells to grow as spheroids, also excludes effects of preformed AGEs by the reaction of glyoxal with fetal calf serum proteins. Our results showed that in cells treated with 200 µM glyoxal, the intercellular contacts in spheroids were disrupted, i.e. cells became totally dissociated. Immunocytochemical analysis revealed a dosedependent accumulation of the AGE product ε N-(carboxymethyl)lysine (CML) in cells detached from cell clusters. The loss of cell attachment was associated with decreased expression of β 1 -integrins and CD44 as revealed by laser scanning cytometry (LSC). Increasing concentrations of glyoxal induced an increase in the number of apoptotic cells which were identified by the immunoreactivity for active caspase-3. Remaining cell clusters showed resistance to both CML formation and apoptosis. The present findings demonstrate that cells treated with glyoxal undergo possibly anoikis, a specific mode of apoptosis caused by loss of cell adhesion.

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“…However, progress in this area has been achieved recently: viruses similar to 229E, the prototype of the initial tissue culture strain, were successfully isolated in human embryonic intestine monolayer cultures from patients with naturally occurring upper respiratory illnesses ; I38 14 virus, the first OC strain, 2 other OC strains LP and EVS, and 229E virus, were recovered in L132 cell monolayers from nasal washings of patients challenged with these agents. In addition, OC43 (and OC38) viruses which were originally recovered in OC and later adapted to grow in suckling mice were not only shown to directly hemagglutinate various erythrocytes but were also adapted to grow in monkey kidney monolayers (2,8,10,12,13). In this paper we have described the hemadsorption of both rat and mouse erythrocytes to various monolayer tissue cultures infected with OC43 virus.…”

Section: Pattern Of Hemadsorptionmentioning

confidence: 94%