scholarly journals Glycoprotein 90K Promotes E-Cadherin Degradation in a Cell Density-Dependent Manner via Dissociation of E-Cadherin–p120-Catenin Complex

2017 ◽  
Vol 18 (12) ◽  
pp. 2601 ◽  
Author(s):  
So-Yeon Park ◽  
Somy Yoon ◽  
Eun Sun ◽  
Rui Zhou ◽  
Jeong Bae ◽  
...  
Keyword(s):  
Cell Density ◽  
Dependent Manner ◽  
P120 Catenin ◽  
Density Dependent ◽  
A Cell ◽  
E Cadherin

scholarly journals Inhibition of transferrin receptor 1 transcription by a cell density response element

2005 ◽  
Vol 392 (2) ◽  
pp. 383-388 ◽  
Author(s):  
Jian Wang ◽  
Guohua Chen ◽  
Kostas Pantopoulos
Keyword(s):  
Cell Density ◽  
Transferrin Receptor ◽  
Human Lung Cancer ◽  
Dependent Manner ◽  
Response Element ◽  
Iron Regulatory Proteins ◽  
Density Dependent ◽  
Transferrin Receptor 1 ◽  
Density Response ◽  
A Cell

TfR1 (transferrin receptor 1) mediates the uptake of transferrin-bound iron and thereby plays a critical role in cellular iron metabolism. Its expression is coupled to cell proliferation/differentiation and controlled in response to iron levels and other signals by transcriptional and post-transcriptional mechanisms. It is well established that TfR1 levels decline when cultured cells reach a high density and in the present study we have investigated the underlying mechanisms. Consistent with previous findings, we demonstrate that TfR1 expression is attenuated in a cell-density-dependent manner in human lung cancer H1299 cells and in murine B6 fibroblasts as the result of a marked decrease in mRNA content. This response is not associated with alterations in the RNA-binding activity of iron regulatory proteins that are indicative of a transcriptional mechanism. Reporter assays reveal that the human TfR1 promoters contains sequences mediating cell-density-dependent transcriptional inhibition. Mapping of the human and mouse TfR1 promoters identified a conserved hexa-nucleotide 5′-GAGGGC-3′ motif with notable sequence similarity to a previously described element within the IGF-2 (insulin-like growth factor-2) promoter. We show that this motif is necessary for the formation of specific complexes with nuclear extracts and for cell-density-dependent regulation in reporter gene assays. Thus the TfR1 promoter contains a functional ‘cell density response element’ (CDRE).

scholarly journals Cell-cell contacts mediated by E-cadherin (uvomorulin) restrict invasive behavior of L-cells.

1991 ◽  
Vol 114 (2) ◽  
pp. 319-327 ◽  
Author(s):  
W C Chen ◽  
B Obrink
Keyword(s):  
Cell Density ◽  
Single Cells ◽  
Cellular Migration ◽  
Dependent Manner ◽  
Collagen Gels ◽  
Cell Contacts ◽  
L Cells ◽  
A Cell ◽  
E Cadherin ◽  
Cell Cell

L-cells were cotransfected with plasmids coding for mouse E-cadherin (uvomorulin) and the neophosphotransferase gene, and stable transfectants expressing E-cadherin at the cell surface were selected and cloned. Control transfection was done with the neophosphotransferase gene alone. The invasive migration of transfected and untransfected L-cells into three-dimensional collagen gels was then analyzed. L-cells not expressing E-cadherin migrated efficiently into the gels, whereas invasion of the E-cadherin-expressing L-cells was restricted in a cell density dependent manner. At sparse density, when the cells exhibited little cell-cell contacts, no difference was observed between the level of invasion of the cadherin-expressing cells and the control cells. However, with increasing cell density, decreasing amounts of the cadherin-expressing cells but increasing amounts of the control cells migrated into the gels. At confluent density hardly any cadherin-expressing cells were able to migrate into the gels. The inhibition of the invasion of the cadherin-expressing cells could be reverted if confluent cells were cultured in the presence of monoclonal antibodies against E-cadherin. Since the expression of E-cadherin did not influence the invasive mobility of single cells, these results indicate that E-cadherin-mediated cell-cell contacts inhibited invasive cellular migration. Time-lapse videoscopy and studies of cell migration from a monolayer into a cell-free area demonstrated that the restricted invasion could be explained by contact inhibition of cell movement of the cadherin-expressing cells.

scholarly journals RalA interacts with ZONAB in a cell density-dependent manner and regulates its transcriptional activity

2004 ◽  
Vol 24 (1) ◽  
pp. 54-62 ◽  
Author(s):  
Paul Frankel ◽  
Ami Aronheim ◽  
Emma Kavanagh ◽  
Maria S Balda ◽  
Karl Matter ◽  
...  
Keyword(s):  
Cell Density ◽  
Transcriptional Activity ◽  
Dependent Manner ◽  
Density Dependent ◽  
A Cell

scholarly journals Cytotoxicity of Brucella smooth strains for macrophages is mediated by increased secretion of the type IV secretion system

Microbiology ◽  
2009 ◽  
Vol 155 (10) ◽  
pp. 3392-3402 ◽  
Author(s):  
Zhijun Zhong ◽  
Yufei Wang ◽  
Feng Qiao ◽  
Zhoujia Wang ◽  
Xinying Du ◽  
...  
Keyword(s):  
Cell Density ◽  
Secretion System ◽  
Effector Proteins ◽  
Type Iv Secretion ◽  
Type Iv Secretion System ◽  
Dependent Manner ◽  
Density Dependent ◽  
Type Iv ◽  
A Cell

Some Brucella rough mutants cause cytotoxicity that resembles oncosis and necrosis in macrophages. This cytotoxicity requires the type IV secretion system (T4SS). In rough mutants, the cell-surface O antigen is shortened and the T4SS structure is thus exposed on the surface. Cytotoxicity effector proteins can therefore be more easily secreted. This enhanced secretion of effector proteins might cause the increased levels of cytotoxicity observed. However, whether this cytotoxicity is unique to the rough mutant and is mediated by overexpression of the T4SS has not been definitively determined. To test this, in the present study, a virB inactivation mutant (BMΔvirB) and an overexpression strain (BM-VIR) of a smooth Brucella melitensis strain (BM) were constructed and their cytotoxicity for macrophages and intracellular survival capability were analysed and compared. Cytotoxicity was detected in macrophages infected with higher concentrations of strains BM or BM-VIR, but not in those infected with BMΔvirB. The quorum sensing signal molecule N-dodecanoyl-dl-homoserine lactone (C12-HSL), a molecule that can inhibit expression of virB, inhibited the cytotoxicity of BM and BM-VIR, but not of BMΔvirB. These results indicated that overexpression of virB is responsible for Brucella cytotoxicity in macrophages. Transcription analysis showed that virB is regulated in a cell-density-dependent manner both in in vitro culture and during macrophage infection. When compared with BM, BM-VIR showed a reduced survival capacity in macrophages and mice, but both strains demonstrated similar resistance to in vitro stress conditions designed to simulate intracellular environments. Taken together, the cytotoxicity of Brucella for macrophages is probably mediated by increased secretion of effector proteins that results from overexpression of virB or an increase in the number of bacterial cells. The observation that both inactivation and overexpression of virB are detrimental for Brucella intracellular survival also indicated that the expression of virB is tightly regulated in a cell-density-dependent manner.

scholarly journals The AinS autoinducer synthase and LitR master regulator of quorum sensing regulate N-3-hydroxy-decanoyl-homoserine-lactone production and motility in Aliivibrio wodanis 06/09/139

2019 ◽  
Author(s):  
Amudha Deepalakshmi Maharajan ◽  
Hilde Hansen ◽  
Nils Peder Willassen
Keyword(s):  
Quorum Sensing ◽  
Cell Density ◽  
Homoserine Lactone ◽  
Temperature Tolerance ◽  
Dependent Manner ◽  
Secretion Systems ◽  
Master Regulator ◽  
Density Dependent ◽  
Ulcer Disease ◽  
A Cell

Abstract Background Quorum Sensing (QS) is a cell to cell communication system, in which bacteria synthesize and respond to signaling molecules called autoinducers (AI). QS is cell density dependent and known to be involved in regulating virulence, motility and secretion systems to interact with the host or other bacteria. Aliivibrio wodanis is frequently isolated together with Moritella viscosa from the infected Atlantic salmon during outbreaks of the winter ulcer disease. M. viscosa is the main causative agent of the disease while the presence of A. wodanis is still unclear. It is hypothesized that A. wodanis might influence the progression of winter ulcer. The genome of A. wodanis 06/09/139 encodes two autoinducer synthase genes (ainS and luxS) and a master regulator litR. LitR homologs in other aliivibrios have been shown to regulate several phenotypes in a cell density dependent manner. Moreover, a previous study has shown that A. wodanis 06/09/139 produces only one AHL N-3-hydroxy-decanoyl-homoserine-lactone (3OHC10-HSL). Hence, in this work, we have studied the QS system in A. wodanis 06/09/139 by knocking out QS genes ainS and litR. The effects of the deletions were studied with regard to growth, AHL production and motility at different temperatures. Results By using HPLC-MS/MS, we found that the deletion of ainS in A. wodanis 06/09/139 resulted in the loss of 3OHC10-HSL production. The 3OHC10-HSL production in A. wodanis 06/09/139 increased with increase in cell density and more 3OHC10-HSL was produced at 6°C than at 12, 16 and 20°C. The litR mutant demonstrated a ~20% reduction in the production of 3OHC10-HSL relative to the wild type at the stationary phase. Compared to the wildtype and the ainS mutant strains, the litR mutant resulted in a strain with improved temperature tolerance. The motility in mutants (∆litR and ∆ainS) were significantly higher than that of the wildtype. Conclusions Our study shows that AinS in A. wodanis 06/09/139 is the AHL synthase responsible for 3OHC10-HSL production, where the production is both cell density and temperature dependent. Our data also shows that LitR regulates 3OHC10-HSL production only to a minor extent and both LitR and AinS are negative regulators of motility.

scholarly journals Cell density-dependent stimulation of PAI-1 and hyaluronan synthesis by TGF-β in orbital fibroblasts

2016 ◽  
Vol 229 (2) ◽  
pp. 187-196 ◽  
Author(s):  
Erika Galgoczi ◽  
Florence Jeney ◽  
Annamaria Gazdag ◽  
Annamaria Erdei ◽  
Monika Katko ◽  
...  
Keyword(s):  
Cell Density ◽  
Inverse Correlation ◽  
Fold Increase ◽  
Dermal Fibroblasts ◽  
Negative Regulator ◽  
Dependent Manner ◽  
Density Dependent ◽  
Cell Densities ◽  
Orbital Fibroblasts ◽  
Pai 1

During the course of Graves’ orbitopathy (GO), orbital fibroblasts are exposed to factors that lead to proliferation and extracellular matrix (ECM) overproduction. Increased levels of tissue plasminogen activator inhibitor type 1 (PAI-1 (SERPINE1)) might promote the accumulation of ECM components. PAI-1 expression is regulated by cell density and various cytokines and growth factors including transforming growth factorβ(TGF-β). We examined the effects of increasing cell densities and TGF-β on orbital fibroblasts obtained from GO patients and controls. Responses were evaluated by the measurement of proliferation, PAI-1 expression, and ECM production. There was an inverse correlation between cell density and the per cell production of PAI-1. GO orbital, normal orbital, and dermal fibroblasts behaved similarly in this respect. Proliferation rate also declined with increasing cell densities. Hyaluronan (HA) production was constant throughout the cell densities tested in all cell lines. In both GO and normal orbital fibroblasts, but not in dermal fibroblasts, TGF-β stimulated PAI-1 production in a cell density-dependent manner, reaching up to a five-fold increase above baseline. This has been accompanied by increased HA secretion and pericellular HA levels at high cell densities. Increasing cell density is a negative regulator of proliferation and PAI-1 secretion both in normal and GO orbital fibroblasts; these negative regulatory effects are partially reversed in the presence of TGF-β. Cell density-dependent regulation of PAI-1 expression in the orbit, together with the local cytokine environment, may have a regulatory role in the turnover of the orbital ECM and may contribute to the expansion of orbital soft tissue in GO.

scholarly journals p120 catenin induces opposing effects on tumor cell growth depending on E-cadherin expression

2008 ◽  
Vol 183 (4) ◽  
pp. 737-749 ◽  
Author(s):  
Edwin Soto ◽  
Masahiro Yanagisawa ◽  
Laura A. Marlow ◽  
John A. Copland ◽  
Edith A. Perez ◽  
...  
Keyword(s):  
Cell Growth ◽  
Tumor Cell ◽  
Mitogen Activated Protein Kinase ◽  
Dependent Manner ◽  
Tumor Cell Growth ◽  
P120 Catenin ◽  
Opposing Effects ◽  
E Cadherin

p120 catenin regulates the activity of the Rho family guanosine triphosphatases (including RhoA and Rac1) in an adhesion-dependent manner. Through this action, p120 promotes a sessile cellular phenotype when associated with epithelial cadherin (E-cadherin) or a motile phenotype when associated with mesenchymal cadherins. In this study, we show that p120 also exerts significant and diametrically opposing effects on tumor cell growth depending on E-cadherin expression. Endogenous p120 acts to stabilize E-cadherin complexes and to actively promote the tumor-suppressive function of E-cadherin, potently inhibiting Ras activation. Upon E-cadherin loss during tumor progression, the negative regulation of Ras is relieved; under these conditions, endogenous p120 promotes transformed cell growth both in vitro and in vivo by activating a Rac1–mitogen-activated protein kinase signaling pathway normally activated by the adhesion of cells to the extracellular matrix. These data indicate that both E-cadherin and p120 are important regulators of tumor cell growth and imply roles for both proteins in chemoresistance and targeted therapeutics.

scholarly journals Expression of the leucocyte common antigen-related (LAR) tyrosine phosphatase is regulated by cell density through functional E-cadherin complexes

2002 ◽  
Vol 365 (2) ◽  
pp. 513-519 ◽  
Author(s):  
Javelle R. SYMONS ◽  
Charles M. LeVEA ◽  
Robert A. MOONEY
Keyword(s):  
Cell Density ◽  
Contact Inhibition ◽  
Mammary Adenocarcinoma ◽  
Low Density ◽  
Common Antigen ◽  
Regulation Of Expression ◽  
Density Dependent ◽  
Protein Levels ◽  
Density Dependent Regulation ◽  
E Cadherin

The leucocyte common antigen-related phosphatase (LAR) has been implicated in receptor tyrosine kinase signalling pathways while also displaying cell-density-dependency and localization to adherens junctions. Whereas physiological substrates for LAR have not been identified unequivocally, β-catenin associates with LAR and is a substrate in vitro. With the implication that LAR may play a role in regulating E-cadherin-dependent cell—cell communication and contact inhibition, the relationship of LAR with E-cadherin was investigated. LAR expression increased with cell density in the human breast cancer cell line MCF-7 and in Ln 3 cells derived from the 13762NF rat mammary adenocarcinoma. LAR protein levels decreased rapidly when cells were replated at a low density after attaining high expression of LAR at high cell density. COS-7 cells displayed comparable density-dependent regulation of LAR expression when transiently expressing exogenous LAR under the control of a constitutively active promoter, indicating that the regulation of expression is not at the level of gene regulation. Disrupting homophilic E-cadherin complexes by chelating extracellular calcium caused a marked decrease in LAR protein levels. Similarly, blocking E-cadherin interactions with saturating amounts of E-cadherin antibody (HECD-1) also led to a rapid and pronounced loss of cellular LAR. In contrast, mimicking cell-surface E-cadherin engagement by plating cells at low density on to dishes coated with HECD-1 resulted in a 2-fold increase in LAR expression compared with controls. These results suggest that density-dependent regulation of LAR expression is mediated by functional E-cadherin and may play a role in density-dependent contact inhibition by regulating tyrosine phosphorylation in E-cadherin complexes.

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