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KSP-positive or -negative cells derived from mouse embryonic stem cells

ABSTRACT: The goals and objectives of this study was to characterize KSP-positive cells derived from mouse embryonic stem cells. KSP is a specific cadherin expressed in renal tubular cells, so it was predicted that KSP-positive cells have characteristics of renal tubular cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE40694 | GEO | 2012/09/07

SECONDARY ACCESSION(S): PRJNA174629

REPOSITORIES: GEO

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KSP-positive or -negative cells derived from mouse embryonic stem cells

Project description:The goals and objectives of this study was to characterize KSP-positive cells derived from mouse embryonic stem cells. KSP is a specific cadherin expressed in renal tubular cells, so it was predicted that KSP-positive cells have characteristics of renal tubular cells. To purify renal lineage cells from differentiated mouse embryonic stem cells, KSP-positive cells were sorted out by use of anti-KSP antibody. Mouse embryonic stem cells were differentiated with Activin 10ng/ml for 18 days through embryoid body formation. 2 independent experiments were carried out. KSP-negative cells were also purified as negative control.

2012-09-07 | E-GEOD-40694 | biostudies-arrayexpress

β-catenin-controlled tubular cell-derived exosomes play a key role in fibroblast activation via the OPN-CD44 axis

Project description:Tubular injury and peripheral fibroblast activation are the hallmarks of chronic kidney disease (CKD) and renal fibrosis, suggesting intimate communication between the two diseases. However, the underlying mechanisms remain to be determined. Exosomes play a role in shuttling proteins and other materials to recipient cells. In our study, we found that tubular cell-derived exosomes were aroused by β-catenin in kidney fibrogenesis. Osteopontin (OPN), especially its N-terminal fragments (N-OPN), was encapsulated in β-catenin-controlled tubular cell-derived exosome cargo, and subsequently passed to fibroblasts. Through binding with CD44, exosomal OPN promoted fibroblast proliferation and activation. Gene deletion of β-catenin in tubular cells (Ksp-β-catenin−/−) or gene ablation of CD44 (CD44−/−) greatly ameliorated renal fibrosis. Notably, N-OPN was secreted by exosome into the urine of patients with CKD, and negatively correlated with kidney function. The urinary exosomes from patients with CKD greatly accelerated renal fibrosis, which was blocked by CD44 deletion. These results suggest that exosome-mediated activation of the OPN/CD44 axis plays a key role in renal fibrosis, which is controlled by β-catenin.

2022-05-20 | PXD030696 | Pride

β-catenin-controlled tubular cell-derived exosomes play a key role in fibroblast activation via the OPN-CD44 axis

2022-12-20 | GSE193282 | GEO

RNA-sequencing shows the changes on transcriptomes after deletion of Setd2 in mice.

Project description:To explore a possible role of SETD2 in kidney development and tumorigenesis in vivo, we generated Setd2-floxed mice and deleted the Setd2 gene in tubular epithelial cells using a transgenic Ksp1.3/Cre mouse line. Then, we established our own c-MYC-transgene mouse line by overexpressing the human c-MYC under the control of the Ksp promoter to generate kidney disease mouse model. To get an insight into the mechanism of how SETD2 ablation promotes ccRCC formation in a c-MYC-generated PKD model, we performed RNA-seq using the renal tubules isolated from Wild Type, Setd2-KO, MYC-OE and MYC-OE; Setd2-KO mice.

2021-03-14 | GSE168849 | GEO

Hippocampal cells multiplex positive and negative engrams

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Hippocampal cells multiplex positive and negative engrams

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CD47 modulates the interaction of γ-catenin with E-cadherin and participates in epithelial–mesenchymal transformation in lipid nephrotoxicity

Project description:Hyperlipidemia, an important risk factor for cardiovascular diseases and end-stage renal disease, often increases renal injury and compromises kidney function. In the present study, the kidney histology analysis in human samples showed that high lipid levels induced renal fibrosis. However, the mechanism of lipid nephrotoxicity remains unknown. We employed mice models of two kinds to further experiments. The kidney histology analysis in mouse showed that high lipid levels induced renal fibrosis that was further confirmed by Western blot and real-time PCR of fibrotic indexes (fibronection, collagenI and α-SMA). In Vitro analysis also supported that OX-LDL significantly induced fibrotic response in HK-2 tubular epithelial cells. To further ascertain the mechanism of high lipid-induced fibrosis, RNA-sequencing (RNA-Seq) was performed. Combined the Gene Ontology (GO) analysis results of differentially expressed mRNAs obtained by RNA-Seq with the results of LC-MS/MS and STRING Functional Association Networks showed that CD47 modulated the interaction of γ-catenin with E-cadherin and participated in epithelial–mesenchymal transformation in lipid nephrotoxicity. The inhibition of CD47 expression by transfected with shRNA plasmid or treated with anti-CD47 antibody in OX-LDL-treated tubular epithelial cells restored the expression of E-cadherin and attenuated renal injury including fibrosis and inflammatory response. These findings indicate that CD47 may be a therapeutic potential target for long-term lipid abuse-induced kidney injury.

2021-03-10 | GSE161737 | GEO

Phosphoproteomcs of the folliculin negative cancer cell line UOK257 +/- lentiviral rescue construct

Project description:In Birt-Hogg-Dubé (BHD) syndrome, germline mutations in the Folliculin (FLCN) gene lead to an increased risk of renal cancer. To address if FLCN is involved regulating cellular signaling pathways via protein and receptor phosphorylation we determined comprehensive phosphoproteomic profiles of FLCN-POS and FLCN-NEG human tumor cells (UOK257). UOK257 misses the folliculin (FLCN) gene, whereas UOK 257-2 harbours a lentiviral rescue of the FLCN gene. Experiment performed in duplicate. This data set is linked to PXD021346 that describes phosphoproteomics results for human renal tubular epithelial cells (RPTEC/TERT1).

2022-07-11 | PXD030237 | Pride

Differentially expressed miRNAs in mice renal tubular epithelial cells which co-cultured with mesenchymal stem cells vs controls

Project description:In order to study the effect of mesenchymal stem cells on miRNAs in renal tubular epithelial cells during renal fibrosis, and to find new treatment methods for renal fibrosis, we used TGF-β1 to stimulate mouse tubular epithelial cells, co-cultured with mesenchymal stem cells for 48 hours, and collected renal tubular epithelial cells .The renal tubular epithelial cells that were only stimulated by TGF-β1 were used as a control group. High-throughput miRNA sequencing was used to detect the increased and decreased miRNAs after co-culture.

2020-04-07 | GSE148144 | GEO

Expression data from mouse EMT-induced and non-induced cells

Project description:The conversion of an epithelial cell to a mesenchymal cell is critical to vertebrate embryogenesis and a defining structural feature of organ development, such as forming fibroblasts in injured tissues, or in initiating metastases in epithelial cancer. From a general perspective, EMT is about disaggregating epithelial units and reshaping epithelia for movement. This phenotypic conversion requires the molecular reprogramming of epithelia with new biochemical instructions. It is known that commonly used molecular markers for EMT include increased expression of N-cadherin and vimentin, nuclear localization of beta-catenin, and increased production of the transcription factors such as Snail, Twist, and SIP1/ZEB2. Much of this conversion, however, has been studied during experiments that expose new transduction and signaling pathways in epithelia, and more recently in fibrogenic tissues. It is not yet clear whether the fibroblast transition of EMT is an expected middle phase of transdifferentiating epithelia, or whether EMT producing fibroblasts is an arrested form of transdifferentiation. EMT is easily engaged by a combination of cytokines associated with proteolytic digestion of basement membranes upon which epithelia reside. We analyzed PCA and hierarchical clustering method of the gene expression pattern of the renal tubular cells and mammary gland cells. We then identified the genes which discriminate between the renal tubular and the mammary gland epithelial cells (PC1), or EMT-induced and non-induced cells (PC3). Undergoing EMT identifies the genes that discriminate between the renal tubular and the mammary gland epithelial cells(PC1), or EMT-induced and non-induced cells (PC3). Affymetrix GeneChip Mouse Genome 430 2.0 Array was used to transcriptionally profile to compare mouse EMT-induced cells and non-induced cells.

2011-08-12 | E-GEOD-31359 | biostudies-arrayexpress

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