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Expression profiling of 3D 2D MDCKII epithelial morphogenesis

ABSTRACT: Formation of epithelial tissues requires the generation of apical-basal polarity and the co-ordination of this polarity between neighboring cells to form a central lumen. MDCK cell line has proven to be a powerful model to study mammalian polarized epithelia in vitro. MDCK cells plated in extracellular matrix (ECM) form cysts, a spherical structure of polarized cells enclosing a central lumen which resembles epithelial tubular structures. The morphogenetic process requires drastic changes in cell architecture, which are regulated by change in gene expression. We used microarrays to identify genes up-regulated in lumen formation. The identification of up-regulated genes could lead us to characterize novel pathways needed for this process.

ORGANISM(S): Canis lupus familiaris

PROVIDER: GSE32495 | GEO | 2011/10/01

SECONDARY ACCESSION(S): PRJNA147767

REPOSITORIES: GEO

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Expression profiling of 3D 2D MDCKII epithelial morphogenesis

Project description:Formation of epithelial tissues requires the generation of apical-basal polarity and the co-ordination of this polarity between neighboring cells to form a central lumen. MDCK cell line has proven to be a powerful model to study mammalian polarized epithelia in vitro. MDCK cells plated in extracellular matrix (ECM) form cysts, a spherical structure of polarized cells enclosing a central lumen which resembles epithelial tubular structures. The morphogenetic process requires drastic changes in cell architecture, which are regulated by change in gene expression. We used microarrays to identify genes up-regulated in lumen formation. The identification of up-regulated genes could lead us to characterize novel pathways needed for this process. MDCKII cells were plated in two different conditions: Cells cultured in confluence in plastic dishes, forming polarized monolayers (2D); or cells cultured in plastic dishes covered with Matrigel (ECM) forming three dimensional cysts (3D). Comparison of both transcriptomic profiles would lead us to identify up-regulated genes in the 3D condition, which would be good candidates to be key regulators of novel processes involved in lumen morphogenesis.

2011-09-30 | E-GEOD-32495 | biostudies-arrayexpress

Identification of genes responsive to change in apical polarity in the breast epithelium

Project description:Differentiation of monolayered epithelia is characterized by the formation of a basoapical polarity axis, except during the early stages of cancer development. Using mammary glandular structures (acini) produced in a three-dimensional cell culture system we have demonstrated that, in order for mammary epithelial cells to exit quiescence and enter the cell cycle, acini have to lose apical polarity. In order to identify the genes dependent on apical polarity that could control cell quiescence, and possibly other aspects of tissue homeostasis, we have used Affymetrix technology microarray analysis of the 22,277 features/genes of the Human Genome U133A 2.0 array Chip in apically polarized and non-polarized breast epithelial acinar cells in three-dimensional culture. Genes commonly down-regulated in two treatments that altered apical polarity compared to control were considered to be dependent on apical polarity status for their transcription. Apically polarized (Control) and two different populations of non-polarized human mammary epithelial cells (18-alpha-glycyrrhetinic acid =AGA, and 5-aza-2'-deoxycytidine =Aza) were used for microarray analysis containing four biological replicates (1-4) for each treatment. The two treatments that cause loss of apical polarity were compared to reference apically polarized control samples using two different statistical analysis methods (FDR and HolmM-bM-^@M-^Ys).

2012-02-29 | E-GEOD-35165 | biostudies-arrayexpress

Identification of genes responsive to change in apical polarity in the breast epithelium

2012-02-29 | GSE35165 | GEO

A survival mechanism controlled by cadherins and Dlg1 polarity complex inhibits Fas cell death receptor signaling

Project description:A fine regulation of epithelia cell death is required to maintain tissue integrity and homeostasis. At a cellular level, this life and death decision is controlled by environmental stimuli including death receptors activation. Here, we show that establishment of cell polarity and AJ formation control the pro-apoptotic signaling emanating from the death receptor Fas. We demonstrate that in colon epithelia Fas concentrates at cell-cell junctions together with the E-cadherin, which protects cells from FasL-induced cell death. The Fas-cadherin association requires the C terminal PDZ binding site of Fas and, using a proteomic approach, we showed that this domain allows the association with the polarity molecule Dlg1. We proved that the interaction of Fas with this scaffold molecule participate to this cell death protection. Therefore inhibition of FasL-induced cell death by Fas-cadherin-Dlg1 complex is a double-edged sword mechanism that helps to maintain epithelial homeostasis by (i) protecting normal polarized epithelia from apoptosis (ii) promoting the elimination of compromised non-polarized cells.

2018-09-20 | PXD009659 | Pride

Spatial transcriptomics reveals a conserved segment polarity program that governs muscle patterning in Nematostella vectensis

Project description:During early animal evolution, the emergence of axially-polarized segments was central to the diversification of complex bilaterian body plans. Nevertheless, precisely how and when segment polarity pathways arose remains obscure. Here we demonstrate the molecular basis for segment polarization in developing larvae of the pre-bilaterian sea anemone Nematostella vectensis. Utilizing spatial transcriptomics, we first constructed a 3-D gene expression atlas of developing larval segments. Capitalizing on accurate in silico predictions, we identified Lbx and Uncx, conserved homeodomain-containing genes that occupy opposing subsegmental domains under the control of both BMP signaling and the Hox-Gbx cascade. Functionally, Lbx mutagenesis eliminated all molecular evidence of segment polarization at larval stage and resulted in an aberrant mirror-symmetric pattern of retractor muscles in primary polyps. These results demonstrate the molecular basis for segment polarity in a pre-bilaterian animal, suggesting that polarized metameric structures were present in the Cnidaria-Bilateria common ancestor over 600 million years ago.

2023-06-12 | GSE173786 | GEO

Nfat5 is involved in the hyperosmotic regulation of Tmem184b, which could be involved in ibuprofen transport in renal MDCK I cells

Project description:Purpose: To investigate the involvement of Nfat5 in the regulation of an ibuprofen transporter Method: Reverse transfection with siRNA against Nfat5 was used to knockdown Nfat5 in MDCK I cells. The uptake of both radiolabelled taurine and ibuprofen was measured in MDCK I cells, first treated with siRNA against Nfat5 for 24 h and afterwards cultivated with raffinose-supplemented normal growth medium (500 mOsm) for 24 h. The knock down of NFat5 was investigated by qpCR and western blotting. A transcriptome analysis of MDCK I cells treated with siRNA against Nfat5 was performed. Validation of the transcriptome analysis was perform with qPCR and radiolabelled uptake of ibuprofen. Results: The siRNA transfection resulted in a knock down of Nfat5, and the uptake of both taurine and ibuprofen was significant decreased in the transfected MDCK I cells. The transcriptome analysis of MDCK I cells treated with siRNA against Nfat5 revealed genes regulated by Nfat5 during hyperosmotic exposure. qPCR and the transciptome analysis showed an involvement of Nfat5 in the hyperosmotic regulation of Tmem184 and uptake in Tmem184b-siRNA treated MDCK I cells showed that Tmem184b might be involved in uptake of ibuprofen. Conclusion: The regulation of Tmem184b was found regulated by Nfat5 and could be a potential possible candidate for the gene product responsible for the uptake of ibuprofen in MDCK I cells

2019-05-10 | GSE122074 | GEO

Mechanisms connecting the conserved protein kinases Kin1, Pom1, and Ssp1 in fission yeast cell polarity and division

Project description:Connections between the protein kinases that function within complex cell polarity networks are poorly understood. Rod-shaped fission yeast cells grow in a highly polarized manner, and genetic screens have identified many protein kinases required for polarized growth and cell shape. Kin1, the sole MARK/PAR-1 family kinase in fission yeast, regulates cell polarity and cytokinesis through unknown mechanisms. We performed a large-scale phosphoproteomics screen to identify and characterize Kin1 substrates in cells.

2017-06-22 | MSV000081185 | MassIVE

QKI regulated splicing required for cell polarity

Project description:QKI regulated splicing required for cell polarity

| PRJNA798365 | ENA

Gene expression profile mediated by independent E-cadherin repressors

Project description:Gene expression profiling of MDCK epithelial cells expressing different repressors (MDCK-Snail, MDCK-Slug and MDCK-E47 cells) versus control MDCK cells. Keywords: Genetic Modification (overexpression of E-cadherin repressors)

2006-11-02 | GSE4151 | GEO

Effect of conditional knockout of Prkci (atypical PKC iota/lambda coding gene) in mouse enterocytes reveals robust innate immunity transcriptomic response

Project description:Atypical PKCiota/lambda is a key effector of the PAR polarity complex which is considered a master determinant of apico-basal polarity in single-layered epithelial cells. In polarized epithelial cells aPKC is exquisitely localized by the PAR6 partner to a belt nearby the tight junctions. Surprisingly, tissue specific knock out of the transgenic floxed version with villin-CRE showed a chronic inflammation phenotype. The observations were made in three different independent transgenic mouse lines and published by three different groups including ours (PMID: 27226486; PMID: 30552022; PMID: 21744423 ), which is reassuring for reproducibility. An additional double KO in both aPKC isoforms further confirmed the results (PMID: 30552022 ). The animals were viable and there was not strong diarrheal or constipation phenotype characteristic of polarity defects in intestinal epithelia. With few exceptions such as ezrin localization, apical polarity markers were generally well polarized. There were changes in cytokine expression by epithelial cells and infiltration of CD8+ T cells (PMID: 27226486; PMID: 30552022). The goal of the study was to get an unbiased catalog of the transcriptional changes induced by aPKC iota/lambda defect in intestinal epithelial cells to understand the ontology of gene expression downstream of the PAR polarity complex. The results are consistent with broad changes in NF-kB and IFN dependent transcriptional pathways, possibly mediated by ROCK and Med17 downstream of aPKCiota/lambda (PMID: 2722648; PMID: 33596087). This study was published in PMID: 33596087.

2023-06-15 | GSE235056 | GEO

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