Expression data from side-population sorted putative intestinal stem cells.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE9013 | GEO | 2007/11/12
SECONDARY ACCESSION(S): PRJNA102501
REPOSITORIES: GEO
Similar Datasets
Project description:While the existence of intestinal epithelial stem cells (IESCs) has been well established, their study has been limited due to the inability to isolate them. Previous work has utilized side population (SP) sorting of the murine small intestinal mucosa to isolate a viable fraction of cells enriched for putative IESCs. We have used microarray analyses to characterize the molecular features of this potential stem cell population. Experiment Overall Design: Fluorescence activated cell sorting of cells stained with Hoechst 33342 and FITC labeled anti-CD45 antibody was used to isolate CD45-/SP and CD45-/nSP cell fractions from mucosal specimens pooled from 3 mice. Intact jejunum specimens were collected prior to sorting. 4 sorts were completed. Therefore, 3 experimental groups were defined: CD45-/SP, CD45-/nSP and intact jejunum, each with 4 biological replicates. Total RNA was extracted from each experiment group for each sort, resulting in 12 specimens submitted for analysis using Affymetrix 430 2.0 Gene Chips.
2008-06-16 | E-GEOD-9013 | biostudies-arrayexpress
Project description:The homeostasis of the gut epithelium relies upon continuous renewal and proliferation of crypt-resident intestinal epithelial stem cells (IESCs). Wnt/β-catenin signaling is required for IESC maintenance, however, it remains unclear how this pathway selectively governs the identity and proliferative decisions of IESCs. Here, we demonstrate that C-terminally-recruited transcriptional co-factors of β-catenin act as all-or-nothing regulators of Wnt-target gene expression. Blocking their interactions with β-catenin rapidly induces loss of IESCs and intestinal homeostasis. Conversely, N-terminally recruited co-factors fine-tune β-catenin’s transcriptional output to ensure proper self-renewal and proliferative behaviour of IESCs. Impairment of N-terminal interactions triggers transient hyperproliferation of IESCs, resulting in exhaustion of the self-renewing stem cell pool. IESC mis-differentiation, accompanied by intrinsic and extrinsic stress signalling results in a process resembling aberrant "villisation" of intestinal crypts. Our data suggest that IESC-specific Wnt/β-catenin output requires discrete regulation of transcription by transcriptional co-factors.
2020-04-21 | GSE148942 | GEO
Project description:The homeostasis of the gut epithelium relies upon continuous renewal and proliferation of crypt-resident intestinal epithelial stem cells (IESCs). Wnt/β-catenin signaling is required for IESC maintenance, however, it remains unclear how this pathway selectively governs the identity and proliferative decisions of IESCs. Here, we demonstrate that C-terminally-recruited transcriptional co-factors of β-catenin act as all-or-nothing regulators of Wnt-target gene expression. Blocking their interactions with β-catenin rapidly induces loss of IESCs and intestinal homeostasis. Conversely, N-terminally recruited co-factors fine-tune β-catenin’s transcriptional output to ensure proper self-renewal and proliferative behaviour of IESCs. Impairment of N-terminal interactions triggers transient hyperproliferation of IESCs, resulting in exhaustion of the self-renewing stem cell pool. IESC mis-differentiation, accompanied by intrinsic and extrinsic stress signalling results in a process resembling aberrant "villisation" of intestinal crypts. Our data suggest that IESC-specific Wnt/β-catenin output requires discrete regulation of transcription by transcriptional co-factors.
2020-04-21 | GSE148941 | GEO
Project description:The homeostasis of the gut epithelium relies upon continuous renewal and proliferation of crypt-resident intestinal epithelial stem cells (IESCs). Wnt/β-catenin signaling is required for IESC maintenance, however, it remains unclear how this pathway selectively governs the identity and proliferative decisions of IESCs. Here, we demonstrate that C-terminally-recruited transcriptional co-factors of β-catenin act as all-or-nothing regulators of Wnt-target gene expression. Blocking their interactions with β-catenin rapidly induces loss of IESCs and intestinal homeostasis. Conversely, N-terminally recruited co-factors fine-tune β-catenin’s transcriptional output to ensure proper self-renewal and proliferative behaviour of IESCs. Impairment of N-terminal interactions triggers transient hyperproliferation of IESCs, resulting in exhaustion of the self-renewing stem cell pool. IESC mis-differentiation, accompanied by intrinsic and extrinsic stress signalling results in a process resembling aberrant "villisation" of intestinal crypts. Our data suggest that IESC-specific Wnt/β-catenin output requires discrete regulation of transcription by transcriptional co-factors.
2020-04-21 | GSE148940 | GEO
Project description:Uterine leiomyoma is the most common benign tumor of the female genital tract, and is the main cause of hysterectomy in 25-30% of affected women. Nevertheless, knowledge about stem cells initiating these common uterine tumors remains scarce. The side population method has been used to identify different somatic stem cells in the human body. In this context, our study explores the hypothesis that human leiomyoma side population cells could be the putative somatic stem cells responsible for leiomyoma's initiation and formation. We isolated, identified and characterized the side population cells from human leiomyomas which implies no commitment to the myometrial lineage at the molecular level, differential cloning efficiency under hypoxic conditions and provides a leiomyoma stem cells gene profile. Based on their cloning efficiency ability, we also established two cell lines (MyoSP1-2) with a normal karyotype under hypoxic conditions. The phenotype analysis supported their mesodermal commitment as assessed by the positive expression of typical mesenchymal markers, such as CD90, CD105, and CD73, and by the absence of hematopoietic stem cell markers like CD34 and CD45. At the mRNA level, we also confirmed their undifferentiated status (OCT-4+, NANOG+, DNMT3B+, GDF3+) and mesenchymal lineage commitment as demonstrated by their ability to differentiate in vitro into adipogenic and osteogenic lineages. Finally, we demonstrated the functional capability of Myo cell lines (MyoSP1-2) to form human leiomyoma-like tissue after injecting this subset of cells either under the kidney capsule or in the subcutaneous tissue in the NOD-SCID mice model. 4 replicates each of leiomyoma side population (SP) cells and leiomyoma total fraction (FT) cells were analyzed.
2012-08-14 | E-GEOD-36157 | biostudies-arrayexpress
Project description:Uterine leiomyoma is the most common benign tumor of the female genital tract, and is the main cause of hysterectomy in 25-30% of affected women. Nevertheless, knowledge about stem cells initiating these common uterine tumors remains scarce. The side population method has been used to identify different somatic stem cells in the human body. In this context, our study explores the hypothesis that human leiomyoma side population cells could be the putative somatic stem cells responsible for leiomyoma's initiation and formation. We isolated, identified and characterized the side population cells from human leiomyomas which implies no commitment to the myometrial lineage at the molecular level, differential cloning efficiency under hypoxic conditions and provides a leiomyoma stem cells gene profile. Based on their cloning efficiency ability, we also established two cell lines (MyoSP1-2) with a normal karyotype under hypoxic conditions. The phenotype analysis supported their mesodermal commitment as assessed by the positive expression of typical mesenchymal markers, such as CD90, CD105, and CD73, and by the absence of hematopoietic stem cell markers like CD34 and CD45. At the mRNA level, we also confirmed their undifferentiated status (OCT-4+, NANOG+, DNMT3B+, GDF3+) and mesenchymal lineage commitment as demonstrated by their ability to differentiate in vitro into adipogenic and osteogenic lineages. Finally, we demonstrated the functional capability of Myo cell lines (MyoSP1-2) to form human leiomyoma-like tissue after injecting this subset of cells either under the kidney capsule or in the subcutaneous tissue in the NOD-SCID mice model.
2012-08-15 | GSE36157 | GEO
Project description:To sum up our results, we managed to isolate a reproducible SP cell fraction of human gastric carcinoma cell lines for the first time. Those cells differed from the rest of the population regarding morphology and biological behaviour. They had the ability to build a population resembling the basic tumor population and therefore performed differenziation and asymmetric cell division. SP cells expressed potential stem cell markers like musashi 1 and Cd133 and also showed a high expression of genes that encode for stem cell properties. The so identified phenotypic and genetic factors showed a variable expression in tumor samples of patient series and might be applicable as prognostic factors in the diagnosis of gastric carcinoma.
2010-12-01 | GSE20058 | GEO
Project description:Mammalian intestinal epithelium stem cells (IESCs) and their daughter cells require the participation of DNA methylation and the transcription factor Sox9 for proliferation and differentiation. Combining methylated DNA immunoprecipitation with microarray hybridization, we demonstrate that hypomethylation in promoter participates in the aberrant formation of crypts in diabetic db/db mice through ectopic Wnt signaling. More importantly, increased expression of Sox9 is accompanied by the loss of methylation in its promoter in IESCs. Using ChIP-seq analysis for Sox9 in IESCs, we demonstrate that Sox9 primarily targets the enhancers of Wnt signaling pathway-related genes. Sox9 is not only predominately acting as a transcriptional activator at proximal enhancer but also as a potential transcriptional inhibitor at distant enhancer. Lack of Sox9 transcriptional activation in specific repressors of Wnt signaling pathway results in loss of intrinsic inhibitory action and ultimately produces over-activation of this pathway in diabetes mellitus.
2017-01-30 | GSE87583 | GEO
Project description:Mammalian intestinal epithelium stem cells (IESCs) and their daughter cells require the participation of DNA methylation and the transcription factor Sox9 for proliferation and differentiation. Combining methylated DNA immunoprecipitation with microarray hybridization, we demonstrate that hypomethylation in promoter participates in the aberrant formation of crypts in diabetic db/db mice through ectopic Wnt signaling. More importantly, increased expression of Sox9 is accompanied by the loss of methylation in its promoter in IESCs. Using ChIP-seq analysis for Sox9 in IESCs, we demonstrate that Sox9 primarily targets the enhancers of Wnt signaling pathway-related genes. Sox9 is not only predominately acting as a transcriptional activator at proximal enhancer but also as a potential transcriptional inhibitor at distant enhancer. Lack of Sox9 transcriptional activation in specific repressors of Wnt signaling pathway results in loss of intrinsic inhibitory action and ultimately produces over-activation of this pathway in diabetes mellitus.
2017-01-30 | GSE87044 | GEO
Project description:A cancer stem cell cannot be identified solely based on surface markers as none of the markers used to isolate stem cells in various normal and cancerous tissues is expressed exclusively by stem cells. Our experimental results have also identified additional fractions representing true stem-like cells in oral squamous cell carcinoma (OSCC), refuting the concept that cancer stem cells (CSCs) are a rare population, and we have also developed an in vitro model to explore the stem cell concept in oral epithelial tumorigenesis. This model expounds four distinct fractions within a homogenous cell line SCC172 that is morphologically similar (85% cells expressing CSC markers), yet varying in all functional aspects of cell cycle, dye retention, chemoresistance, tumor-forming potential, self renewal, apoptosis resistance and regulation at molecular levels. Relating to our CSC shift model, we analysed the concept of biological heterogeneity in terms of four fractions SP1, SP2, MP1 and MP2 and associated it with variations among patients in a clinical scenario.
2016-12-31 | GSE36111 | GEO