scholarly journals The rotavirus surface protein VP8 modulates the gate and fence function of tight junctions in epithelial cells

2004 ◽  
Vol 117 (23) ◽  
pp. 5509-5519 ◽  
Author(s):  
P. Nava
Keyword(s):  
Epithelial Cells ◽  
Tight Junctions ◽  
Surface Protein ◽  
Fence Function

scholarly journals Claudin-4 Reconstituted in Unilamellar Vesicles is Sufficient to Form Tight Interfaces that Partition Membrane Proteins

2018 ◽  
Author(s):  
Brian Belardi ◽  
Sungmin Son ◽  
Michael D. Vahey ◽  
Jinzhi Wang ◽  
Jianghui Hou ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Membrane Proteins ◽  
Epithelial Cells ◽  
Tight Junctions ◽  
Direct Evidence ◽  
Accessory Proteins ◽  
Unilamellar Vesicles ◽  
Outer Leaflet ◽  
Fence Function

AbstractTight junctions have been hypothesized to act as molecular fences in the plasma membrane of epithelial cells, helping to form differentiated apical and basolateral domains. While this fence function is believed to arise from the interaction of four-pass transmembrane claudins, the complexity of tight junctions has made direct evidence of their role as a putative diffusion barrier difficult to obtain. Here we address this challenge by reconstituting claudin-4 into giant unilamellar vesicles using microfluidic jetting. We find that reconstituted claudin-4 is sufficient to form adhesive interfaces between unilamellar vesicles without accessory proteins present in vivo. By controlling the molecular composition of the inner and outer leaflets of jetted membranes, we show that claudin-4-mediated interfaces can drive partitioning of extracellular membrane proteins but not of inner or outer leaflet lipids. Our findings indicate that homotypic interactions of claudins and their small size can contribute to the polarization of epithelial cells.

ZO-2 silencing in epithelial cells perturbs the gate and fence function of tight junctions and leads to an atypical monolayer architecture

2007 ◽  
Vol 313 (8) ◽  
pp. 1533-1547 ◽  
Author(s):  
Sandra Hernandez ◽  
Bibiana Chavez Munguia ◽  
Lorenza Gonzalez-Mariscal
Keyword(s):  
Epithelial Cells ◽  
Tight Junctions ◽  
Fence Function

Tight Junctions of Human Uterine Epithelial Cells Change during the Menstrual Cycle: A Morphometric Study

1992 ◽  
Vol 144 (1) ◽  
pp. 36-38 ◽  
Author(s):  
C.R. Murphy ◽  
P.A.W. Rogers ◽  
M.J. Hosie ◽  
J. Leeton ◽  
L. Beaton
Keyword(s):  
Menstrual Cycle ◽  
Epithelial Cells ◽  
Tight Junctions ◽  
Morphometric Study ◽  
Uterine Epithelial Cells

The effect of berberine in vitro on tight junctions in human Caco-2 intestinal epithelial cells

Fitoterapia ◽  
2009 ◽  
Vol 80 (4) ◽  
pp. 241-248 ◽  
Author(s):  
Lili Gu ◽  
Ning Li ◽  
Qiurong Li ◽  
Qiang Zhang ◽  
Chengyang Wang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Tight Junctions ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial

scholarly journals Structural and Functional Regulation of Tight Junctions by RhoA and Rac1 Small GTPases

1998 ◽  
Vol 142 (1) ◽  
pp. 101-115 ◽  
Author(s):  
Tzuu-Shuh Jou ◽  
Eveline E. Schneeberger ◽  
W. James Nelson
Keyword(s):  
Tight Junctions ◽  
Spatial Organization ◽  
Mdck Cells ◽  
Protein Localization ◽  
Freeze Fracture ◽  
Tracer Diffusion ◽  
Small Gtpases ◽  
Dominant Negative ◽  
Solute Diffusion ◽  
Fence Function

Tight junctions (TJ) govern ion and solute diffusion through the paracellular space (gate function), and restrict mixing of membrane proteins and lipids between membrane domains (fence function) of polarized epithelial cells. We examined roles of the RhoA and Rac1 GTPases in regulating TJ structure and function in MDCK cells using the tetracycline repressible transactivator to regulate RhoAV14, RhoAN19, Rac1V12, and Rac1N17 expression. Both constitutively active and dominant negative RhoA or Rac1 perturbed TJ gate function (transepithelial electrical resistance, tracer diffusion) in a dose-dependent and reversible manner. Freeze-fracture EM and immunofluoresence microscopy revealed abnormal TJ strand morphology and protein (occludin, ZO-1) localization in RhoAV14 and Rac1V12 cells. However, TJ strand morphology and protein localization appeared normal in RhoAN19 and Rac1N17 cells. All mutant GTPases disrupted the fence function of the TJ (interdomain diffusion of a fluorescent lipid), but targeting and organization of a membrane protein in the apical membrane were unaffected. Expression levels and protein complexes of occludin and ZO-1 appeared normal in all mutant cells, although ZO-1 was more readily solubilized from RhoAV14-expressing cells with Triton X-100. These results show that RhoA and Rac1 regulate gate and fence functions of the TJ, and play a role in the spatial organization of TJ proteins at the apex of the lateral membrane.

Impaired Localization of Claudin-11 in Endometriotic Epithelial Cells Compared to Endometrial Cells

2018 ◽  
Vol 26 (9) ◽  
pp. 1181-1192 ◽  
Author(s):  
Fabian Horné ◽  
Raimund Dietze ◽  
Eniko Berkes ◽  
Frank Oehmke ◽  
Hans-Rudolf Tinneberg ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Tight Junctions ◽  
Cell Lines ◽  
Human Cancer ◽  
Deep Infiltrating Endometriosis ◽  
Endometrial Cell ◽  
Ovarian Endometriosis ◽  
Eutopic Endometrium ◽  
Endometrial Cells ◽  
Ectopic Endometrium

Claudins are the major components of tight junctions and are often deregulated in human cancer, permitting escape of cancer cells along with the acquisition of invasive properties. Similarly, endometrial cells also show invasive capabilities; however, the role of tight junctions in endometriosis has only rarely been examined. In this study, we analyzed the protein expression and localization of claudin-7 and claudin-11 in human eutopic and ectopic endometrium and endometrial cell lines. We identified claudin-7 primarily at the basolateral junctions of the glandular epithelial cells in eutopic endometrium as well as in the ectopic lesions in nearly all glands and cysts. Quantification of claudin-7 localization by HSCORE showed a slight increase in peritoneal and deep infiltrating endometriosis (DIE) compared to eutopic endometrium. In contrast, claudin-11 was localized mainly in the apicolateral junctions in nearly all glandular epithelial cells of the eutopic endometrium. Interestingly, we observed a deregulation of claudin-11 localization to a basal or basolateral localization in ovarian ( P < .001), peritoneal ( P < .01), and DIE ( P < .05) and a moderately decreased abundance in ovarian endometriosis. In endometrial cell lines, claudin-7 was only present in epithelial Ishikawa cells, and silencing by small-interfering RNA increased cell invasiveness. In contrast, claudin-11 could be demonstrated in Ishikawa and endometriotic 12Z and 49Z cells. Silencing of claudin-11 decreased invasiveness of 12Z slightly but significantly in 49Z. We suggest that although claudin-7 and claudin-11 can be found in nearly all eutopic and ectopic epithelial cells, the impaired localization of claudin-11 in ectopic endometrium might contribute to the pathogenesis of endometriosis.

scholarly journals Mechanosensitive calcium signaling promotes epithelial tight junction remodeling by activating RhoA

2021 ◽  
Author(s):  
Saranyaraajan Varadarajan ◽  
Rachel E. Stephenson ◽  
Eileen R. Misterovich ◽  
Jessica L. Wu ◽  
Ivan S. Erofeev ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Intracellular Calcium ◽  
Tight Junctions ◽  
Calcium Influx ◽  
Cell Junctions ◽  
Mechanical Stimuli ◽  
Local Repair ◽  
Transient Activation ◽  
Epithelial Tight Junction ◽  
Sense And Respond

Epithelia maintain an effective barrier by remodeling cell-cell junctions in response to mechanical stimuli. Cells often respond to mechanical stress through activating RhoA and remodeling actomyosin. Previously, we found that local leaks in the barrier are rapidly repaired by localized, transient activation of RhoA – ″Rho flares″ – but how Rho flares are initiated remains unknown. Here, we discovered that intracellular calcium flashes occur in Xenopus laevis epithelial cells undergoing Rho flare-mediated remodeling of tight junctions. Calcium flashes originate at the site of barrier leaks and propagate into the cell. Depletion of intracellular calcium or inhibition of mechanosensitive calcium channels (MSC) reduced the amplitude of calcium flashes and diminished the activation of Rho flares. Furthermore, MSC-dependent calcium influx was necessary to maintain global barrier function by regulating local repair of tight junctions through efficient junction contraction. We propose that MSC-dependent calcium flashes are an important mechanism allowing epithelial cells to sense and respond to local leaks induced by mechanical stimuli.

scholarly journals Role of nectin in organization of tight junctions in epithelial cells

2002 ◽  
Vol 7 (10) ◽  
pp. 1059-1072 ◽  
Author(s):  
Atsunori Fukuhara ◽  
Kenji Irie ◽  
Akio Yamada ◽  
Tatsuo Katata ◽  
Tomoyuki Honda ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Tight Junctions

scholarly journals Sorting of Marburg Virus Surface Protein and Virus Release Take Place at Opposite Surfaces of Infected Polarized Epithelial Cells

2001 ◽  
Vol 75 (3) ◽  
pp. 1274-1283 ◽  
Author(s):  
Christian Sänger ◽  
Elke Mühlberger ◽  
Elena Ryabchikova ◽  
Larissa Kolesnikova ◽  
Hans-Dieter Klenk ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Apical Membrane ◽  
Basolateral Membrane ◽  
Surface Protein ◽  
Hemorrhagic Fever ◽  
Marburg Virus ◽  
Virus Surface ◽  
Mdckii Cells ◽  
Vesicular Stomatitis ◽  
Polarized Epithelial Cells

ABSTRACT Marburg virus, a filovirus, causes severe hemorrhagic fever with hitherto poorly understood molecular pathogenesis. We have investigated here the vectorial transport of the surface protein GP of Marburg virus in polarized epithelial cells. To this end, we established an MDCKII cell line that was able to express GP permanently (MDCK-GP). The functional integrity of GP expressed in these cells was analyzed using vesicular stomatitis virus pseudotypes. Further experiments revealed that GP is transported in MDCK-GP cells mainly to the apical membrane and is released exclusively into the culture medium facing the apical membrane. When MDCKII cells were infected with Marburg virus, the majority of GP was also transported to the apical membrane, suggesting that the protein contains an autonomous apical transport signal. Release of infectious progeny virions, however, took place exclusively at the basolateral membrane of the cells. Thus, vectorial budding of Marburg virus is presumably determined by factors other than the surface protein.

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