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Transcriptional profiles of human islet and exocrine endothelial cells in subjects with or without impaired glucose metabolism

ABSTRACT: We report the application of RNA sequencing to quantify the global transcriptome of sorted endothelial cells from the endocrine and exocrine pancreas in normoglycemic and impaired glucose metabolism(IGM) human donors.

ORGANISM(S): Homo sapiens

PROVIDER: GSE157546 | GEO | 2021/01/25

REPOSITORIES: GEO

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Transcriptional profiles of human islet and exocrine endothelial cells in subjects with or without impaired glucose metabolism.

Project description:In experimental studies, pancreatic islet microvasculature is essential for islet endocrine function and mass, and islet vascular morphology is altered in diabetic subjects. Even so, almost no information is available concerning human islet microvascular endothelial cell (MVEC) physiology and gene expression. In this study, islets and exocrine pancreatic tissue were acquired from organ donors with normoglycemia or impaired glucose metabolism (IGM) immediately after islet isolation. Following single-cell dissociation, primary islet- and exocrine MVECs were obtained through fluorescence-activated cell sorting (FACS) and transcriptional profiles were generated using AmpliSeq. Multiple gene sets involved in general vascular development and extracellular matrix remodeling were enriched in islet MVEC. In exocrine MVEC samples, multiple enriched gene sets that relate to biosynthesis and biomolecule catabolism were found. No statistically significant enrichment was found in gene sets related to autophagy or endoplasmic reticulum (ER) stress. Although ample differences were found between islet- and exocrine tissue endothelial cells, no differences could be observed between normoglycemic donors and donors with IGM at gene or gene set level. Our data is consistent with active angiogenesis and vascular remodeling in human islets and support the notion of ongoing endocrine pancreas tissue repair and regeneration even in the adult human.

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Transcription profiling of cultured normal human islet tissue, islets treated with interferon alpha 2 beta, islet-depleted exocrine pancreas, pancreas, liver and kidney tissue

Project description:The purpose of this study was to identify mRNA transcripts encoding tissue restricted cell surface proteins on human islet tissue that, in turn, might serve as markers for determination of healthy, transplanted and/or diseased islet cell mass. Using oligonucleotide microarrays and clinical grade human islets, we obtained the gene expression profiles of cultured normal islet tissue and compared them to profiles of islets treated with interferon alpha 2 beta, islet-depleted exocrine pancreas, pooled whole pancreas, pooled liver and pooled kidney tissue. Data set filtering and comparisons of gene expression patterns revealed a small set of genes corresponding to transmembrane or membrane associated proteins with limited tissue distributions (present in Islets of Langerhans and, often, central or peripheral nervous system tissues, but absent from exocrine pancreas, liver, kidney and other tissues) with possible utility as novel islet markers. Under the influence of IFN alpha, some of these transcripts show differential expression as confirmed by real time PCR. In addition, we found significant differential expression of two sets of transcripts expressed in islets but with broad tissue distributions, non classical MHC class I b (HLA-G and F) and MHC Class II locus (e.g. HLA-DR alpha and HLA-DQ alpha and beta).

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LRH-1 and PTF1-L coregulate an exocrine pancreas-specific transcriptional network for digestive function

Project description:This SuperSeries is composed of the following subset Series: GSE34030: LRH-1 and PTF1-L coregulate an exocrine pancreas-specific transcriptional network for digestive function [RNA-Seq] GSE34295: LRH-1 and PTF1-L coregulate an exocrine pancreas-specific transcriptional network for digestive function [ChIP-Seq] Refer to individual Series

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Transcriptional profiles of human islet and exocrine endothelial cells in subjects with or without impaired glucose metabolism

Project description:Transcriptional profiles of human islet and exocrine endothelial cells in subjects with or without impaired glucose metabolism

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Age-associated DNA methylation increases in mouse pancreatic islets suggest an epigenetic drift toward the exocrine pancreas epigenome

Project description:Early postnatal overnutrition causes persistent dysregulation of endocrine pancreas function. We used genome-scale DNA methylation profiling in the suckling-period small litter (SL) mouse model to test whether this occurs via persistent epigenetic changes in pancreatic islets. Although SL islets showed DNA methylation changes directly after weaning and in adulthood, few of these were present at both ages, contrary to our hypothesis. Most interestingly, we discovered that genomic regions that are hypermethylated in exocrine relative to endocrine pancreas tend to gain methylation in islets during aging. Focusing on a subset of genes relevant to β cell function, we showed that these methylation differences are strongly correlated with expression. Together, our results provide the novel insight that DNA methylation changes that occur as islets age indicate an overall epigenetic drift toward the exocrine pancreas epigenome. These concerted shifts in the islet methylome could contribute to the age-associated decline in endocrine pancreas function. Pancreatic islets were isolated from P21/P180 SL or C mice. To ensure purity of islets, 3 rounds of manual picking were performed in each samples. Whole pancreas samples, ~98% of which is exocrine pancreas, were used as exocrine pancreas. There are 5 mice per group.

2014-12-03 | E-GEOD-63811 | biostudies-arrayexpress

LRH-1 and PTF1-L coregulate an exocrine pancreas-specific transcriptional network for digestive function [ChIP-Seq]

Project description:We have determined the cistrome and transcriptome for the nuclear receptor liver receptor homolog-1 (LRH-1) in the exocrine pancreas. Chromatin immunoprecipitation (ChIP)-seq and RNA-seq analyses reveal that LRH-1 directly induces expression of genes encoding digestive enzymes and secretory and mitochrondrial proteins. LRH-1 cooperates with the pancreas transcription factor 1-L complex (PTF1-L) in regulationg exocrine pancreas-specific gene expression. Elimination of LRH-1 in adult mice reduced the concentration of several lipases and proteases in pancreatic fluid and impaired pancreatic fluid secretion in response to cholecystokinin. Thus, LRH-1 is a key regulator of the exocrine pancreas-specific transcriptional network required for the production and secretion of pancreatic fluid. input and Lrh1 ChIP

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LRH-1 and PTF1-L coregulate an exocrine pancreas-specific transcriptional network for digestive function [ChIP-Seq]

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PERK role in the exocrine pancreas

Project description:Molecular characterization of PERK's role in the mouse exocrine pancreas. Postnatal days 16, 19 and 32 were examined. Postnatal day 16 represents a stage immediately prior to severe cytological changes in the exPKO mice. Postnatal day 19 represents the initial stage of severe phenotypes in the exPKO mice. Postnatal day 32 represents the middle stage of severe phenotypes (about 2 wks from the initiation) in the exPKO mice. Keywords: transgenic mouse

2007-08-01 | GSE4422 | GEO

Age-associated DNA methylation increases in mouse pancreatic islets suggest an epigenetic drift toward the exocrine pancreas epigenome

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A single cell atlas of the murine pancreatic ductal tree identifies novel cell populations with potential implications in pancreas regeneration and exocrine pathogenesis.

Project description:Pancreatic ducts form an intricate network of tubules that secrete bicarbonate and drive acinar secretions into the duodenum. This network is formed by centroacinar cells, terminal, intercalated, intracalated ducts, and the main pancreatic duct. Ductal heterogeneity at the single-cell level has been poorly characterized. Here, we used scRNA-seq to comprehensively characterize mouse ductal heterogeneity at single-cell resolution of the entire ductal epithelium from centroacinar cells to the main duct. Moreover, we used organoid cultures, injury models and pancreatic tumor samples to interrogate the role of novel ductal populations in pancreas regeneration and exocrine pathogenesis. In our study, we have identified the coexistence of 15 ductal populations within the healthy pancreas and characterized their organoid formation capacity and endocrine differentiation potential. Cluster isolation and subsequent culturing let us identify ductal cell populations with high organoid formation capacity and endocrine and exocrine differentiation potential in vitro, including Wnt-responsive-population, ciliated-population and FLRT3+ cells. Moreover, we have characterized the location of these novel ductal populations in healthy pancreas, chronic pancreatitis and tumor samples, hightlihgting a putative role of WNT-responsive, IFN-responsive and EMT-populations in pancreatic exocrine pathogenesis as their expression inceases in chronic pancreatitis and PanIN lesions. In light of our discovery of previously unidentified ductal populations, we unmask the potential roles of specific ductal populations in pancreas regeneration and exocrine pathogenesis.

2024-03-24 | GSE262292 | GEO

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