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The microRNA-200 family regulates pancreatic beta-cell survival in type 2 diabetes (islet)

ABSTRACT: Islets from control and beta-cell specific miR-141/200c overexpressing mice were extracted and Affymetrix gene expression analysis performed We used Affymetrix Chip analysis to address which genes are regulated upon miR-200-overexpression in beta-cells at the age of 6 weeks.

ORGANISM(S): Mus musculus

PROVIDER: GSE58488 | GEO | 2015/05/06

SECONDARY ACCESSION(S): PRJNA252783

REPOSITORIES: GEO

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The microRNA-200 family regulates pancreatic beta-cell survival in type 2 diabetes (islet)

Project description:Islets from control and beta-cell specific miR-141/200c overexpressing mice were extracted and Affymetrix gene expression analysis performed We used Affymetrix Chip analysis to address which genes are regulated upon miR-200-overexpression in beta-cells at the age of 6 weeks. Transgenic mice overexpressing miR-141/200c and control mice were subjected to islet extraction, RNA was extracted using Trizol method, and Affymetrix analysis was performed.

2015-05-06 | E-GEOD-58488 | biostudies-arrayexpress

The microRNA-200 family regulates pancreatic beta-cell survival in type 2 diabetes (Min6 cells)

Project description:The microRNAs miR-141 and -200c were co-overexpressed in the Min6 beta-cell line, which caused pro-apoptotic gene expression and subsquently apoptosis. We used Affymetrix Chip analysis to address which genes are regulated upon miR-200-overexpression to define target genes of miR-200 and pro-apoptotic genes upregulated by miR-200 to induce apoptosis. Min6 cells were infected with a control Adenovirus or Adenovirus overexpression miR-141/200c. Cells were harvested with Trizol and RNA extraction was performed. RNA from n=3 wells was pooled for each condition and subjected to Affymetrix chip analysis

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The microRNA-200 family regulates pancreatic beta-cell survival in type 2 diabetes (Min6 cells)

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Project description:We performed RNA sequencing of islets of Langerhans isolated from RipmiR-141~200c and RipmiR-141~200c Zeb1200M mice to determine the transcriptomic effects of mutating miR-200 binding sites in the endogenous Zeb1 3'UTR of mice in which miR-141~200c is overexpressed under the rat insulin promoter (RIP).

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Global changes in gene expression in response to miR-200 overexpression in 4TO7 cells

Project description:Transcriptional profiling of 4TO7 cells stably overexpressing miR-200s or CDH1. We observe a dramatic shift in the gene signatures when miR-200s (cluster 2; miR-200c/141, or both clusters) are overexpressed relative to controls. However, cluster 1 overexpression (miRs-200b/a/429) alone or CDH1 overexpression does not induce global changes in gene expression to levels observed for cluster 2 (miR-200c/141) or both clusters together. One cell line (4TO7) cells: four different overexpression experiments, Cluster 1, Cluster 2, Clusters 1+2, CDH1, and respective controls, Puro vec, Hygro vec, Puro+Hygro vec and Puro vec. Each experiment has two biological replicates. Total, 16 samples.

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MicroRNA-200c/141 confines ERα activity and expression pattern by targeting Ccnd1 [single-cell RNA-seq]

Project description:ERα is one of the most important transcription factors and therapeutic targets in breast cancer. The patterns of ERα expression in normal breast tissue and cancerous lesions are strikingly different. What drives the change of ERα pattern during lesions formation remains unclear. Here, we describe a novel regulatory mechanism through which miR-200c/141 regulates the level as well as the distribution of ERα in the mammary gland. miR-200c/141 is specifically expressed in luminal cells. Luminal-deletion of miR-200c/141 (miR-cKO) leads to a drastic expansion of ERα+ cell proportion. Single cell RNAseq reveals that miR-cKO generates aberrant luminal subpopulations with increased proliferative and anti-apoptotic features. In vivo lineage tracing of ER- luminal cells demonstrates that miR-200c/141 deletion can convert ER- cells into ER+ cells, which contribute partly to the increase of ERα+ luminal cells. Mechanistic study identifies Ccnd1 as a novel target of miR-200c/141 . Upon miR-200c/141deletion, elevated Ccnd1 level corroborates ERα transcriptional activation, leads to enhanced ERα signaling activity, consequently increased transcription of ERα coding gene Esr1 through self-activation at promoter E1. Our findings reveal a new miR-200c/141-Ccnd1-ERα axis, and provide new molecular insights into how miR-200c/141-Ccnd1 enforces the lineage barrier between ER- and ER+ luminal cells, and what drives the change of ERα expression pattern.

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MicroRNA-200c/141 confines ERα activity and expression pattern by targeting Ccnd1 [bulk RNA-seq]

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Project description:Islet samples were sequenced to determine the effect of miR-200 KO or miR-200 site mutation in Zeb1 on tumorigenesis in RT2 mice; re-expression of individual miR-200 family members in miR-200KO cells was performed to determine the individual roles of miR-141 and miR-200c seeds

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The Pitx2:miR-200c/141:noggin pathway regulates BMP signaling and ameloblast differentiation

Project description:The mouse incisor is a remarkable tooth that grows throughout the animal’s lifetime. This continuous renewal is fueled by epithelial stem cells that give rise to ameloblasts, which generate enamel, and little is known about the function of specific miRNAs in this process. Here we describe the role of a novel Pitx2:miR-200c/141:Noggin regulatory pathway in dental epithelial cell differentiation. miR-200c repressed noggin, an antagonist of Bmp signaling. Pitx2 expression caused an up-regulation of miR-200c and chromatin immunoprecipitation (ChIP) assays revealed endogenous Pitx2 binding to the miR-200c/141 promoter. A positive feedback loop was discovered between miR-200c and Bmp signaling. miR-200c/141 induced expression of E-cadherin and the dental epithelial cell differentiation marker, amelogenin. In addition, miR-203 expression was activated by endogenous Pitx2 and targeted the Bmp antagonist Bmper to further regulate Bmp signaling. miR-200c/141 knockout mice showed defects in enamel formation with decreased E-cadherin and amelogenin expression and increased noggin expression. Our in vivo and in vitro studies reveal a multistep transcriptional program involving the Pitx2:miR-200c/141:Noggin regulatory pathway that is important in epithelial cell differentiation and tooth development.

2013-07-09 | GSE48583 | GEO

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