Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1083287 | ENA |
REPOSITORIES: ENA
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Project description:The gastrointestinal (GI) epithelium is a highly regenerative tissue with the potential to provide a renewable source of insulin+ cells using cellular reprogramming. Here, we describe the antral stomach as a previously unrecognized source highly amenable to conversion into functional insulin-secreting cells. Native antral endocrine cells share a surprising degree of transcriptional similarity with pancreatic beta-cells. Expression of beta-cell reprogramming factors in vivo converts antral cells efficiently into insulin+ cells with close molecular and functional resemblance to beta-cells. Our data further indicate that the intestine-expressed Cdx2 acts as a molecular barrier for beta-cell conversion. Induced GI insulin+ cells can suppress hyperglycemia over at least 6 months and they regenerate rapidly after ablation from the native stem-cell compartment. Transplantation of bioengineered stomach mini-organs also produced insulin+ cells and suppressed hyperglycemia. These studies demonstrate the potential of developing engineered stomach tissue as a renewable source of functional beta-cells for glycemic control. Total RNA extracted from primary mouse tissues: Stomach (3 replicates), Duodenum (3 replicates) and Colon (2 replicates)
2016-01-09 | E-GEOD-76686 | biostudies-arrayexpress
Project description:The gastrointestinal (GI) epithelium is a highly regenerative tissue with the potential to provide a renewable source of insulin+ cells using cellular reprogramming. Here, we describe the antral stomach as a previously unrecognized source highly amenable to conversion into functional insulin-secreting cells. Native antral endocrine cells share a surprising degree of transcriptional similarity with pancreatic beta-cells. Expression of beta-cell reprogramming factors in vivo converts antral cells efficiently into insulin+ cells with close molecular and functional resemblance to beta-cells. Our data further indicate that the intestine-expressed Cdx2 acts as a molecular barrier for beta-cell conversion. Induced GI insulin+ cells can suppress hyperglycemia over at least 6 months and they regenerate rapidly after ablation from the native stem-cell compartment. Transplantation of bioengineered stomach mini-organs also produced insulin+ cells and suppressed hyperglycemia. These studies demonstrate the potential of developing engineered stomach tissue as a renewable source of functional beta-cells for glycemic control.
2016-01-09 | GSE76686 | GEO
Project description:VCF for 87 Argentinean samples. Only SNPs (no indels) that passed the Affymetrix QC. Data from Luisi et al. 2020. Plos One. Fine-Scale Genomic Analyses Of Admixed Individuals Reveal Unrecognized Genetic Ancestry Components In Argentina. Reference Allele column does NOT contain reference allele from genome assembly.
| EGAD00001006227 | EGA
Project description:Diverse functions of the homeodomain transcription factor BARX1 include Wnt-dependent, non-cell autonomous specification of the stomach epithelium, tracheo-bronchial septation, and Wnt-independent expansion of the spleen primordium. Tight spatio-temporal regulation of Barx1 levels in the mesentery and stomach mesenchyme suggests additional roles. To determine these functions, we forced constitutive BARX1 expression in the Bapx1 expression domain, which includes the mesentery and intestinal mesenchyme, and also examined Barx1-/- embryos in further detail. Transgenic embryos invariably showed intestinal truncation and malrotation, in part reflecting abnormal left-right patterning. Ectopic BARX1 expression did not affect intestinal epithelium, but intestinal smooth muscle developed with features typical of the stomach wall. BARX1, which is normally restricted to the developing stomach, drives robust smooth muscle expansion in this organ by promoting proliferation of myogenic progenitors at the expense of other sub-epithelial cells. Undifferentiated embryonic stomach and intestinal mesenchyme showed modest differences in mRNA expression and BARX1 was sufficient to induce much of the stomach profile in intestinal cells. However, limited binding at cis-regulatory sites implies that BARX1 may act principally through other transcription factors. Genes expressed ectopically in BARX1+ intestinal mesenchyme and reduced in Barx1-/- stomach mesenchyme include Isl1, Pitx1, Six2 and Pitx2, transcription factors known to control left-right patterning and influence smooth muscle development. The sum of evidence suggests that potent BARX1 functions in intestinal rotation and stomach myogenesis occur through this small group of intermediary transcription factors.
2015-06-03 | GSE69483 | GEO