Epithelial-mesenchymal interactions in uterus and vagina alter the expression of the cell surface proteoglycan, syndecan

Boutin, Eugenie L.; Sanderson, Ralph D.; Bernfield, Merton; Cunha, Gerald R.

doi:10.1016/0012-1606(91)90317-v

Cited by 56 publications

(31 citation statements)

References 37 publications

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“…Differential expression of the LGV-or trachoma-specific secondary receptors in vivo would reflect the pathologies associated with each biovar. A similar hypothesis has been proposed by Wyrick and colleagues (28), attributing the colonization and infection of the submucosal layer by the L2 serovar, which is primarily a submucosal pathogen, to the enrichment of HS in the extracellular matrix (4). In addition to restricted cell surface expression of HS, one could also envision the secondary receptor providing an additional level of specificity that further defines the differences in pathology associated with LGV and non-LGV serovars.…”

supporting

confidence: 58%

“…Briefly, cells were fixed with freshly prepared 4% paraformaldehyde for 40 min at room temperature. The cells were rinsed with phosphate-buffered saline three times, and the remaining paraformaldehyde was neutralized by incubation with 10 mM NH 4 Cl for 30 min at 4°C, followed by an incubation with 3% bovine serum albumin for 30 min at 4°C. The inhibition of chlamydial internalization was confirmed by electron microscopy (data not shown).…”

mentioning

confidence: 99%

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Isolation and Characterization of a Mutant Chinese Hamster Ovary Cell Line That Is Resistant to Chlamydia trachomatis Infection at a Novel Step in the Attachment Process

Carabeo¹,

Hackstadt²

2001

Infect Immun

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Host factors involved in Chlamydia trachomatis pathogenesis were investigated by random chemical mutagenesis of Chinese hamster ovary (CHO-K1) cells followed by selection for clones resistant to chlamydial infection. A clonal mutant cell line, D4.1-3, refractory to infection by the C. trachomatis L2 serovar was isolated. The D4.1-3 cell line appears to be lacking in a previously undescribed temperature-dependent and heparinresistant binding step that occurs subsequent to engagement of cell surface heparan sulfate by L2 elementary bodies. This novel binding step differentiates the lymphogranuloma venereum (LGV) serovar from other serovars and may contribute the different pathologies associated with LGV and non-LGV strains.Strains of Chlamydia trachomatis are the etiologic agents of the most common form of sexually transmitted disease in the United States and of preventable blindness worldwide (21). Chlamydiae are obligate intracellular parasites that possess a unique biphasic life cycle. Infection of a host cell is initiated by the elementary body (EB), which is a metabolically inactive form, while multiplication is achieved by the noninfectious but metabolically active reticulate body. Intracellular survival of chlamydiae occurs within a specialized parasitophorous vacuole, termed an inclusion, that is neither acidified nor fusogenic with lysosomes (18). After infection, an EB very quickly dissociates itself from the endosomal/lysosomal pathway and translocates to the peri-Golgi region, where it begins to intercept exocytic vesicle containing sphingomyelin. The processes of dissociation and translocation depend on chlamydial de novo transcription and synthesis of proteins that are thought to modify the inclusion membrane leading to restricted fusogenicity with the lysosomes (11,12,22).Because of the obligate intracellular nature of chlamydiae, the ability to attach to and enter susceptible host cells is an unconditional requirement. Presently, relatively little is known about the chlamydial entry process. Their obligate intracellular lifestyle, coupled with a lack of a genetic system, poses a formidable barrier in identifying the virulence factors involved in the pathogenesis of this organism. One of the principal virulence factors that would indeed be of great importance in understanding chlamydial pathogenesis, as well as offering a potential target for prophylactic intervention, is the bacterial adhesin. Presently, a number of distinct surface molecules have been proposed to function as adhesins in the attachment of chlamydiae to host cells. They include the major outer membrane protein (23, 24), heat shock protein 70 (Hsp70) (20), OmcB (Omp2) (26), and heparan sulfate (HS)-like glycosaminoglycans (GAGs) (29). Definitive identification of the virulence factors continues to be a challenge.A number of laboratories have attempted to complement this approach by examining the chlamydial infection process from the perspective of the host cell. Like many viral and bacterial pathogens, some chlamydiae have been shown...

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confidence: 58%

mentioning

confidence: 99%

Isolation and Characterization of a Mutant Chinese Hamster Ovary Cell Line That Is Resistant to Chlamydia trachomatis Infection at a Novel Step in the Attachment Process

Carabeo¹,

Hackstadt²

2001

Infect Immun

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“…Within squamous epithelia that undergo regeneration, syndecan-1 expression is lost in the most highly differentiated cells [41]. During embryonic development syndecan-1 is also expressed by various mesenchymal cells, especially during periods of critical epithelium-mesenchyme interactions [42][43][44][45][46]. Syndecan-1 has been shown to be expressed by pre-B-cells in the bone marrow, but expression is lost immediately before the mature B-cells are released into the circulation [47].…”

Section: Expression Of Syndecansmentioning

confidence: 99%

Syndecans: multifunctional cell-surface co-receptors

Carey

1997

Biochemical Journal

621

497

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This review will summarize our current state of knowledge of the structure, biochemical properties and functions of syndecans, a family of transmembrane heparan sulphate proteoglycans. Syndecans bind a variety of extracellular ligands via their covalently attached heparan sulphate chains. Syndecans have been proposed to play a role in a variety of cellular functions, including cell proliferation and cell–matrix and cell–cell adhesion. Syndecan expression is highly regulated and is cell-type- and developmental-stage-specific. The main function of syndecans appears to be to modulate the ligand-dependent activation of primary signalling receptors at the cell surface. Principal functions of the syndecan core proteins are to target the heparan sulphate chains to the appropriate plasma-membrane compartment and to interact with components of the actin-based cytoskeleton. Several functions of the syndecans, including syndecan oligomerization and actin cytoskeleton association, have been localized to specific structural domains of syndecan core proteins.

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“…Syndecan-1 has been suggested to be a morphoregulatory molecule because its expression during embryonic development is dynamically regulated and corresponds to morphological boundaries (9). Changes in syndecan-1 expression correlate with morphologic changes during interactions between epithelial and mesenchymal cells in tooth (10), kidney (11), female reproductive tract (12), and limb bud (13) development.…”

mentioning

confidence: 99%

Syndecan-1 Expression Is Down-regulated during Myoblast Terminal Differentiation

Larraı́n¹,

Cizmeci-Smith²,

Troncoso³

et al. 1997

Journal of Biological Chemistry

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Syndecan-1 is an integral membrane proteoglycan involved in the interaction of cells with extracellular matrix proteins and growth factors. It is transiently expressed in several condensing mesenchymal tissues after epithelial induction. In this study we evaluated the expression of syndecan-1 during skeletal muscle differentiation. The expression of syndecan-1 as determined by Northern blot analyses and immunofluorescence microscopy is down-regulated during differentiation. The transcriptional activity of a syndecan-1 promoter construct is also down-regulated in differentiating muscle cells. The decrease in syndecan-1 gene expression is not dependent on the presence of E-boxes, binding sites for the MyoD family of transcription factors in the promoter region, or myogenin expression. Deletion of the region containing the E-boxes or treatment of differentiating cells with sodium butyrate, an inhibitor of myogenin expression, had no effect on syndecan-1 expression. Basic fibroblast growth factor and transforming growth factor type ␤, which are inhibitors of myogenesis, had little effect on syndecan-1 expression. When added together, however, they induced syndecan-1 expression. Retinoic acid, an inducer of myogenesis, inhibited syndecan-1 expression and abolished the effect of the growth factors. These results indicate that syndecan-1 expression is down-regulated during myogenesis and that growth factors and retinoic acid modulate syndecan-1 expression by a mechanism that is independent of myogenin.

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Epithelial-mesenchymal interactions in uterus and vagina alter the expression of the cell surface proteoglycan, syndecan

Cited by 56 publications

References 37 publications

Isolation and Characterization of a Mutant Chinese Hamster Ovary Cell Line That Is Resistant to Chlamydia trachomatis Infection at a Novel Step in the Attachment Process

Isolation and Characterization of a Mutant Chinese Hamster Ovary Cell Line That Is Resistant to Chlamydia trachomatis Infection at a Novel Step in the Attachment Process

Syndecans: multifunctional cell-surface co-receptors

Syndecan-1 Expression Is Down-regulated during Myoblast Terminal Differentiation

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