Regulation of E-cadherin expression by dexamethasone and tumour necrosis factor-α in nasal epithelium

Carayol, Nathalie; Vachier, Isabelle; Campbell, Alison M.; Crampette, L.; Bousquet, Jean; Godard, P.; Chanez, Pascal

doi:10.1183/09031936.02.00013602

Cited by 26 publications

(23 citation statements)

References 30 publications

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“…While all associations occurred during ICS use, associations with epithelial E-cadherin expression were significant for five SNPs in the absence of ICSs. These results may indicate that ICSs may influence the way these polymorphisms express their effect and are consistent with in vitro results showing that administration of glucocorticosteroids can upregulate cadherin expression, improve cell-cell contact and strengthen the epithelial barrier [19,21,22].…”

Section: Discussionsupporting

confidence: 88%

“…Additionally, we used FEV1/ vital capacity (VC) ratio post-bronchodilation (BD) adjusted for sex, age, height and smoking as a marker of remodelling in both populations [17]. Since E-cadherin expression is known to be upregulated by ICSs [13,18,19], we tested for interaction between ICS and genotypes by introducing interaction terms into the models. General (heterozygotes versus wild types and homozygous mutants versus wild types) genetic models were used.…”

Section: Statisticsmentioning

confidence: 99%

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E-cadherin gene polymorphisms in asthma patients using inhaled corticosteroids

et al. 2011

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E-cadherins form intercellular junctions that maintain epithelial integrity. Epithelial integrity is impaired in asthma and can be restored by inhaled corticosteroids (ICSs). Our aim was to investigate the association of CDH1 gene polymorphisms (single-nucleotide polymorphisms (SNPs)) with airway remodelling, inflammation and forced expiratory volume in 1 s (FEV1) decline in asthma patients and assess whether ICSs modulate these effects.Bronchial biopsies of 138 asthmatics were available (population 1). Associations of 17 haplotype-tagging SNPs with epithelial E-cadherin expression, biopsy parameters and FEV1/vital capacity (VC) ratio were tested. FEV1 and VC data were collected in 281 asthmatics with 30-yr follow-up (population 2). Linear mixed-effect models were used to assess associations of SNPs with FEV1 decline.Seven out of the 17 SNPs were associated with airway remodelling, three with CD8+ T-cell counts, two with eosinophil counts and seven with FEV1 decline. All associations occurred only in patients using ICS. In general, alleles associated with less remodelling correlated with less FEV1 decline and higher FEV1/VC. Decreased epithelial E-cadherin expression was associated with five SNPs in non-ICS users.In conclusion, our data show that CDH1 polymorphisms are associated with epithelial Ecadherin expression and suggest that epithelial adhesion is an important contributor to airway remodelling and lung function in asthma. These effects are modified by the use of inhaled corticosteroids.

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Section: Discussionsupporting

confidence: 88%

Section: Statisticsmentioning

confidence: 99%

E-cadherin gene polymorphisms in asthma patients using inhaled corticosteroids

et al. 2011

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“…Beneath direct cell contacts, attachment of epithelial cells to extracellular matrix is known to provide a survival signal, in which GC-induced activity of the survival kinase PI3-K/Akt is suggested to be involved [165]. Binding of E-cadherin, a molecule involved in adhesion between epithelial cells, may play a role in preventing apoptosis, as examined in granulosa cells [166] and in nasal epithelial cells, in which GCs induced expression of E-cadherin [167].…”

Section: Tissue Formation As a Mediator Of Gc-induced Resistance In Cmentioning

confidence: 97%

Regulation of differential pro- and anti-apoptotic signaling by glucocorticoids

et al. 2006

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More than a quarter of a century ago, the phenomenon of glucocorticoid-induced apoptosis in the majority of hematological cells was first recognized. More recently, glucocorticoid-induced antiapoptotic signaling associated with apoptosis resistance has been identified in cells of epithelial origin, most of malignant solid tumors and some other tissues. Despite these huge amount of data demonstrating differential pro- and anti-apoptotic effects of glucocorticoids, the underlying mechanisms of cell type specific glucocorticoid signaling are just beginning to be described. This review summarizes our present understanding of cell type-specific pro- and anti-apoptotic signaling induced by glucocorticoids. In the first section we give a summary and update of known glucocorticoid-induced pathways mediating apoptosis in hematological cells. We shortly introduce mechanisms of glucocorticoid resistance of hematological cells. We highlight and discuss the emerging molecular evidence of a general induction of survival signaling in epithelial cells and carcinoma cells by glucocorticoids. We provide a model for glucocorticoid-induced resistance in cells growing in a tissue formation. Thus, attachment to the extracellular matrix and cell-cell contacts typical for e.g. epithelial and tumor cells may be crucially involved in switching the balance of several interacting pathways to survival upon treatment with glucocorticoids.

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“…The dysfunction of ß-catenin/Ecadherin complex is suggested to mediate as a factor for the invasiveness and destructive growth of tumour cells into adjacent tissue because of a resulting loss of regular cell adhesion (18). Carayol et al induced a decrease in ß-catenin expression in human nasal epithelial tissue by TNF-α (19). This decrease was inhibited by the addition of dexamethasone (19).…”

Section: Introductionmentioning

confidence: 99%

“…Carayol et al induced a decrease in ß-catenin expression in human nasal epithelial tissue by TNF-α (19). This decrease was inhibited by the addition of dexamethasone (19).…”

Section: Introductionmentioning

confidence: 99%

Influence of interleukin-13 on β-catenin levels ineosinophilic chronic rhinosinusitis cell culture

Sauter¹,

Stern‐Straeter²,

Chang³

et al. 2008

Int J Mol Med

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Abstract. Chronic rhinosinusitis (CRS) is one of the most common chronic diseases. The etiology and classification of CRS, with and without nasal polyps, remain unclear. Eosinophils and their products are important in the pathophysiology of allergic diseases and in host immunity to certain organisms. Interleukin 13 (IL-13) plays a pivotal role in eosinophilic inflammation. The migration of epithelial cells requires permanent re-establishment of the intercellular connection. Intercellular connections are maintained by the modulation of adherens junctions consisting of an E-cadherin/ß-catenin complex. In our study we examined the eosinophilic and non-eosinophilic paranasal mucosa obtained from two patients undergoing functional endoscopic sinus surgery. Cell cultures were incubated with human recombinant IL-13 for up to 72 h and ß-catenin concentration was determined with ELISA techniques. Furthermore, immunostaining for ß-catenin was used for the semi-quantitative description of specimens. We were able to ascertain a significant increase in ß-catenin expression in the eosinophilic paranasal cell culture after IL-13 administration compared to the non-eosinophilic culture. Immunostaining for ß-catenin was restricted to the membrane of the cells. Concerning the increased mural expression of ß-catenin, we presume that a fibrotic reaction similar to asthma and chronic obstructive pulmonary disease occurs in patients suffering from CRS. Furthermore, ß-catenin overexpression might be responsible for mucosal thickening and IL-13 seems to be an important marker in eosinophilic CRS.

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Regulation of E-cadherin expression by dexamethasone and tumour necrosis factor-α in nasal epithelium

Cited by 26 publications

References 30 publications

E-cadherin gene polymorphisms in asthma patients using inhaled corticosteroids

E-cadherin gene polymorphisms in asthma patients using inhaled corticosteroids

Regulation of differential pro- and anti-apoptotic signaling by glucocorticoids

Influence of interleukin-13 on β-catenin levels ineosinophilic chronic rhinosinusitis cell culture

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