Tumour necrosis factor-α-mediated dyscohesion of epithelial cells is associated with disordered expression of cadherin/β-catenin and disassembly of actin filaments

Tabibzadeh, Siamak; Kong, Q.F.; Kapur, Suman; Satyaswaroop, P.G.; Aktories, Klaus

doi:10.1093/molehr/1.2.74

Cited by 26 publications

(19 citation statements)

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“…VE cadherin has been shown to be a major component of the endothelial adherens junction, which maintains and modulates vascular permeability [29][30][31][32]. Studies showed that VE cadherin is a target of inflammatory mediators during cytokine-induced permeability and EC gap formation [33,34]. Our data showed that HMGB1 decreased the amount of VE cadherin in cell membrane surface and induced intercellular gap formation.…”

Section: Discussionsupporting

confidence: 52%

HMGB1 Increases Permeability of the Endothelial Cell Monolayer via RAGE and Src Family Tyrosine Kinase Pathways

Huang

Liu

et al. 2011

Inflammation

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High-mobility group box 1 (HMGB1) was recently established as a proinflammatory mediator of sepsis, and its potential role in the pathogenesis of sepsis remains elusive. In the present study, we determined whether HMGB1 increases the permeability of the endothelial cell monolayer in sepsis. Permeability was measured from fluorescein isothiocyanate (FITC)-dextran 40-kDa flux across the endothelial cell monolayer at control and after HMGB1 administration. We found that HMGB1 increased human umbilical vein endothelial cell permeability to FITC-dextran 40 kDa in a time- and concentration-dependent manner. HMGB1 induced the mRNA transcription and protein expression of receptor for advanced glycation end products (RAGE). Blockade of cell surface receptors RAGE with specific neutralizing antibodies and RAGE siRNA or blockade of Src family tyrosine kinase with inhibitor PP2 significantly reduced HMGB1-induced hyperpermeability of endothelial cell monolayer. Our data demonstrate that (1) HMGB1 increases permeability of endothelial cell monolayer in a time- and concentration-dependent manner and (2) HMGB1-induced hyperpermeability is mediated through RAGE and Src family tyrosine kinase signaling pathway. These findings may have implications for therapeutic interventions in patients with sepsis.

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Section: Discussionsupporting

confidence: 52%

HMGB1 Increases Permeability of the Endothelial Cell Monolayer via RAGE and Src Family Tyrosine Kinase Pathways

Huang

Liu

et al. 2011

Inflammation

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“…The direct impairment of TJ function triggered by TNF-α was reported in a number of epithelial cell lines [46,47]. Disordered E-cadherin/ beta-catenin and disassembly of actin filaments were found to be responsible for the TNF-α-stimulated ECC1 endometrial cell dyscohesion [48]. However, ZO-1 distribution was unaffected due to the incubation with TNF-α in HT-29/B6 cells [49].…”

Section: Discussionmentioning

confidence: 99%

Acute Oxidative Stress Affects IL-8 and TNF-α Expression in IPEC-J2 Porcine Epithelial Cells

et al. 2011

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Reactive oxygen species are implicated in cell and tissue damage in a number of diseases including acute and chronic inflammation of the gut. Effects of H(2)O(2) exposure on non-carcinogenic porcine epithelial cell line, IPEC-J2 cells cultured on collagen-coated membrane inserts were monitored based on transepithelial electrical resistance (TER) change, extent of necrotic cell damage, gene expression of inflammatory cytokines IL-8 and TNF-α. Furthermore, the junction proteins claudin-1 and E-cadherin were also investigated by immunohistochemistry. Peroxide (1mM) increased IL-8 and TNF-α gene expression levels significantly allowing 1 h recovery time without affecting the cellular distribution of junction proteins, TER and cell survival rate. In conclusion, the IPEC-J2 cell line on membrane insert was introduced as a fast and reliable investigation tool for oxidative stimuli-triggered intestinal inflammation and in the future as a screening method for antioxidant and probiotic candidates.

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“…The other two TJ-integral membrane proteins, occludin and claudin-11, have also been shown to be downregulated by TNF␣ in HT-29/B6 [74] and in mouse Sertoli cells [75], respectively. In addition, TNF␣ downregulates E-cadherin and ␤-catenin in celiac disease [76]. Furthermore, TNF␣ was shown to perturb the Sertoli cell TJ-barrier function in vitro [38].…”

Section: Tnf␣ and Junction Dynamicsmentioning

confidence: 97%

Extracellular Matrix: Recent Advances on Its Role in Junction Dynamics in the Seminiferous Epithelium During Spermatogenesis1

Siu

Cheng

2004

Biology of Reproduction

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Spermatogenesis takes place in the seminiferous epithelium of the mammalian testis in which one type A1 spermatogonium (diploid, 2n) gives rise to 256 spermatids (haploid, 1n). To accomplish this, developing germ cells, such as preleptotene and leptotene spermatocytes, residing in the basal compartment of the seminiferous epithelium must traverse the blood-testis barrier (BTB) entering into the adluminal compartment for further development into round, elongating, and elongate spermatids. Recent studies have shown that the basement membrane in the testis (a modified form of extracellular matrix, ECM) is important to the event of germ cell movement across the BTB because proteins in the ECM were shown to regulate BTB dynamics via the interactions between collagens, proteases, and protease inhibitors, possibly under the regulation of cytokines. While these findings are intriguing, they are not entirely unexpected. For one, the basement membrane in the testis is intimately associated with the BTB, which represents the basolateral region of Sertoli cells. Also, Sertoli cell tight junctions (TJs) that constitute the BTB are present side-by-side with cell-cell actin-based adherens junctions (AJ, such as basal ectoplasmic specialization [ES]) and intermediate filament-based desmosome-like junctions. As such, the relative morphological layout between TJs, AJs, and desmosome-like junctions in the seminiferous epithelium is in sharp contrast to other epithelia where TJs are located at the apical portion of an epithelium or endothelium, furthest away from ECM, to be followed by AJs and desmosomes, which in turn constitute the junctional complex. For another, anchoring junctions between a cell epithelium and ECM found in multiple tissues, also known as focal contacts (or focal adhesion complex, FAC, an actin-based cell-matrix anchoring junction type), are the most efficient junction type that permits rapid junction restructuring to accommodate cell movement. It is therefore physiologically plausible, and perhaps essential, that the testis is using some components of the focal contacts to regulate rapid restructuring of AJs between Sertoli and germ INTRODUCTIONDuring spermatogenesis, preleptotene and leptotene spermatocytes residing at the basal compartment of the seminiferous epithelium adjacent to the basement membrane must traverse the blood-testis barrier (BTB) at late stage VIII through early stage IX of the epithelial cycle, entering the adluminal compartment for further development ( Figs. 1 and 2) [1][2][3]. These primary spermatocytes continue to differentiate into round, elongating, and eventually elongate spermatids while moving to the luminal edge of the epithelium and to be released into the tubule lumen at spermiation [2]. These events of cell movement across the seminiferous epithelium are also associated with extensive remodeling of actin-based cell-cell and cell-matrix anchoring junctions, also known as adherens junctions (AJs) and focal contacts, respectively; as well as intermediate filament-based ...

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Tumour necrosis factor-α-mediated dyscohesion of epithelial cells is associated with disordered expression of cadherin/β-catenin and disassembly of actin filaments

Cited by 26 publications

References 0 publications

HMGB1 Increases Permeability of the Endothelial Cell Monolayer via RAGE and Src Family Tyrosine Kinase Pathways

HMGB1 Increases Permeability of the Endothelial Cell Monolayer via RAGE and Src Family Tyrosine Kinase Pathways

Acute Oxidative Stress Affects IL-8 and TNF-α Expression in IPEC-J2 Porcine Epithelial Cells

Extracellular Matrix: Recent Advances on Its Role in Junction Dynamics in the Seminiferous Epithelium During Spermatogenesis1

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