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Global Proteomic Analysis of E-cadherin Function in Mouse Embryonic Stem Cells Using iTRAQ and LC-MS/MS

ABSTRACT: This project identifies all the proteomic changes that take place in mouse embryonic stem cells after the knockout of the cell-cell adhesion protein E-cadherin. It identifies several putative pathways and sheds the light on the role of E-cadherin in controlling metabolsim of these pluripotent stem cells. The downregulation of E-cadherin resulted in the inhibiton of mitochondrial complex III and the upregulation of HIF-alpha-1 targets

INSTRUMENT(S): QSTAR

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Cell Culture, Embryonic Stem Cell

SUBMITTER: Aseel Sharaireh

LAB HEAD: Dr Richard Unwin

PROVIDER: PXD012679 | Pride | 2020-07-09

REPOSITORIES: Pride

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			Action	DRS
	20160516_AS_D3_ECADNULL_A08.wiff	Wiff
	20160516_AS_D3_ECADNULL_A08.wiff.scan	Wiff
	20160516_AS_D3_ECADNULL_A09.wiff	Wiff
	20160516_AS_D3_ECADNULL_A09.wiff.scan	Wiff
	20160516_AS_D3_ECADNULL_A10.wiff	Wiff

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Publications

Epithelial cadherin regulates transition between the naïve and primed pluripotent states in mouse embryonic stem cells.

Sharaireh Aseel M AM Fitzpatrick Lorna M LM Ward Chris M CM McKay Tristan R TR Unwin Richard D RD

Stem cells (Dayton, Ohio) 20200704 10

Inhibition of E-cad in mouse embryonic stem cells (mESCs) leads to a switch from LIF-BMP to Activin/Nodal-dependent pluripotency, consistent with transition from a naïve to primed pluripotent phenotype. We have used both genetic ablation and steric inhibition of E-cad function in mESCs to assess alterations to phenotype using quantitative mass spectrometry analysis, network models, and functional assays. Proteomic analyses revealed that one third of detected proteins were altered in E-cad null m ...[more]

PMID: 32621788

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Pharmacological HIF-1 activation synergically upregulated exosome production with adiponectin through induction and stabilization of T-cadherin

Project description:Purpose: Addition of HIF-PH inhibitor, Roxadustat upregulate and stabilize T-cadherin protein. The purpose is to investigate whether genes induced by HIF-PH inhibitors are involved in the regulation of T-cadherin. Methods: mRNA of F2T cells, murine endotherial cell line stably overexpressed T-cadhetin supplemented with or without Adiponectin and/or Roxadustat were sequenced on Illumina NovaSeq 6000 (Illumina). Total RNA qualities were analysised using RNA6000 pico kit (Agilent) and we confirmed that RNA integrity number of samples were 6.5 or more. Data analysis was performed using iDEP ve.1.1 or Biojupies on web application. Results: We identified about 1,000 genes upregulated by addition of Roxadustat. In KEGG pathway analysis, we especially focused on cell adhesion and ECM-receptor interaction among upregulated genes.

2024-02-21 | GSE242647 | GEO

Effect of E-cadherin by N-cadherin replacement in mouse intestinal epithelial cells

Project description:We conditionally substituted E-cadherin (E-cad; cadherin 1) with N-cadherin (N-cad; cadherin 2) during intestine development by generating mice in which an Ncad cDNA was knocked into the Ecad locus We used microarray to follow gene expression changes derived from lack of E-cadherin on intestinal epithelial cells

2017-05-01 | GSE81920 | GEO

Bulk RNA sequencing of VE-Cadherin+GFP+, VE-Cadherin- GFP+ and VE-Cadherin+GFP- populations from E11.5 miR144/451+/GFP mouse yolk sac.

Project description:The aim of the experiment was to compare a newly defined population VE-Cadherin+GFP+ to control populations, VE-Cadherin- GFP+ and VE-Cadherin+GFP-.

2019-04-20 | GSE113403 | GEO

Transcription profile of adipose derived mesenchymal stem cells separated by cell surface protein N-cadherin.

2013-10-29 | GSE35232 | GEO

Muscle stem cell niche localization, quiescence, and maintenance are cadherin-dependent but separable functions

Project description:Adhesion between stem cells and their niche promotes stable niche localization and provides signaling information to sustain properties such as quiescence. Skeletal muscle stem cells (MuSCs) are localized between an adjacent myofiber and an enwrapping basal lamina. The most abundant cadherin in MuSCs, M-cadherin, is dispensable for MuSC function, whereas N-cadherin is required to prevent MuSCs from breaking quiescence in the absence of injury. Loss of both cadherins exacerbates this phenotype, yet the MuSCs remain in the niche and maintain regenerative function. These findings raise the possibility that cadherins are dispensable for anchorage of MuSCs to their niche. To address this question, we conditionally removed from MuSCs b- and g-catenin and, separately, aE- and aT-catenin, factors essential for cadherin-dependent adhesion. Catenin-deficient MuSCs break quiescence similarly to N-/M-cadherin-deficient MuSCs, but exit the niche, and are depleted via a single fate: precocious differentiation, reentry to the niche, and fusion to myofibers. These findings indicate that separable, cadherin-dependent functions are required in MuSCs for niche localization, quiescence, and stem cell maintenance.

2024-03-07 | GSE244181 | GEO

Transcription profile of adipose derived mesenchymal stem cells separated by cell surface protein N-cadherin.

Project description:Mesenchymal stem cells (MSCs) are one of most promising stem cell sources for regenerative medicine. MSCs have a differention ability into several tissues. However, their differentiation efficiency is considered quite limited. Especially, the differentiation efficiency into cardiomyocytes is very low. N-cadherin is one of the cell surface protein that is expressed in developing and adult cardiomyocytes. We found that cell surface expression of N-cadherin in MSCs shows good correlation with the cardiomyogenic differentiation ability. We also analyzed the expression profiles of N-cadherin-positive and N-cadherin-negative fraction by microarray. We found that N-cadherin-positive MSCs show higher expression of some of the cardiomyogenesis-related genes than N-cadherin-negative MSCs. The ASCs were maintained in MesenPRO RSTM Medium. The ASCs were harvested in a cell dissociation buffer. The ASCs were incubated with biotinylated anti N-cadherin antibody and next incubated with streptavidin M-bM-^@M-^SAPC. Subsequently cells were incubated with anti-APC microbeads. Immunomagnetic separation of N-cadherin+ cells were performed with autoMACSTMPro separator applying the separation program M-bM-^@M-^Xdepl025M-bM-^@M-^Y

2013-10-29 | E-GEOD-35232 | biostudies-arrayexpress

Expression data from three endothelial cell lines derived from murine embryonic stem cells expressing VE-cadherin, N-cadherin or both

Project description:Endothelial cells (ECs) express two members of the cadherin family, VE- and N-cadherin. While VE-cadherin induces EC homotypic adhesion, N-cadherin function in ECs remains largely unknown. EC-specific inactivation of either VE- or N-cadherin leads to early foetal lethality suggesting that these cadherins play a non-redundant role in vascular development. Goal of this study was to further investigate this hypothesis analyzing both additive and divergent functions of the two cadherins in ECs.

2012-01-10 | GSE34948 | GEO

Transcription profiling by array of mouse wild type and E-cadherin knockout embryonic stem cells grown with or without cytokine leukemia inhibitory factor

Project description:We previously observed that E-cadherin knockout embryonic stem cells do not differentiate in the absence of the cytokine leukemia inhibitory factor (LIF) (Soncin et al., 2009, Stem Cells 27 p2069-2080). This experiment was designed to compare the transcription profile of E-cadherin KO ES cells cultured in the presence and absence of LIF. We also compared E-cadherin KO ES cells with wild type D3 ES cells grown in the presence of LIF.

2011-06-19 | E-MEXP-2836 | biostudies-arrayexpress

E-cadherin interactome complexity and robustness resolved by quantitative proteomics

Project description:E-cadherin-mediated cell-cell adhesion and signaling plays an essential role in development and maintenance of healthy epithelial tissues. Adhesiveness mediated by E-cadherin is conferred by its extracellular cadherin domains and is regulated by an assembly of adaptors and enzymes associated with its cytoplasmic tail. Here, we used proximity biotinylation and quantitative proteomics to identify 561 proteins in the vicinity of E-cadherin’s cytoplasmic tail. Isolation of E-cadherin-mediated adhesion plaques from a cell-glass interface added positional context to the proteomic results. Moreover, using expression of GFP-tagged fusion proteins, we determine the subcellular localization of 83 of the E-cadherin proximal proteins, and identify 24 novel adherens junction components. We employed a structure-informed database of protein-protein interactions to construct a comprehensive E-cadherin interactome, containing 82 known and 419 previously uncharacterized proteins. Finally, we found that calcium chelation did not disrupt most protein interactions with E-cadherin, suggesting that most E-cadherin interactions are independent of cell-cell adhesion.

2016-07-06 | PXD000448 | Pride

Transcription profiling of mouse embryonic stem cells expressing VE-cadherin (CD144) during endothelial differentiation

Project description:Endothelial differentiation occurs during normal vascular development in the developing embryo. Mouse embryonic stem (ES) cells were used to further define the molecular mechanisms of endothelial differentiation. By flow cytometry a population of VEGF-R2 positive cells was identified as early as 2.5 days after differentiation of ES cells, and a subset of VEGF-R2 + cells, that were CD41+ positive at 3.5 days. A separate population of VEGF-R2+ stem cells expressing the endothelial-specific marker CD144 (VE-cadherin) was also identified at this same time point. Microarray analysis of >45,000 transcripts was performed on RNA obtained from cells expressing VEGF-R2, CD41, and CD144. Experiment Overall Design: We identified four populations of cells; cells expressing VEGF-R2 (day 2.5), CD41 expressing cells (day 3.5), cells expressing CD144 (VE-Cadherin, day 3.5), and cells expressing CD144 (day 6.5). In addition to this, we have also obtained the negative control cells at each time such as VEGF-R2 (day 2.5) negative, CD41 negative (day 3.5), CD144 negative (VE-Cadherin, day 3.5), and negative CD144 (day 6.5). RNA for the microarray experiments were obtained in duplicate from two separately conducted experiments using the murine embryonic stem cells..

2008-10-20 | E-GEOD-10210 | biostudies-arrayexpress

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