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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of pancreatic islets from Hnf1a-deficient and wild type mice

ABSTRACT: Pancreatic islets were isolated from Hnf1a (Hepatocyte nuclear factor 1 alpha) knockout and wild-type mice and cultured ex vivo for two days in RPMI medium with 10% FBS before RNA extraction. The transcription profiles were obtained using Affymetrix GeneChip Mouse Genome 430A 2.0 arrays [Mouse430A_2].

ORGANISM(S): Mus musculus

SUBMITTER: Joan-Marc Servitja

PROVIDER: E-MEXP-1707 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Hnf1alpha (MODY3) controls tissue-specific transcriptional programs and exerts opposed effects on cell growth in pancreatic islets and liver.

Servitja Joan-Marc JM Pignatelli Miguel M Maestro Miguel Angel MA Cardalda Carina C Boj Sylvia F SF Lozano Juanjo J Blanco Enrique E Lafuente Amàlia A McCarthy Mark I MI Sumoy Lauro L Guigó Roderic R Ferrer Jorge J

Molecular and cellular biology 20090316 11

Heterozygous HNF1A mutations cause pancreatic-islet beta-cell dysfunction and monogenic diabetes (MODY3). Hnf1alpha is known to regulate numerous hepatic genes, yet knowledge of its function in pancreatic islets is more limited. We now show that Hnf1a deficiency in mice leads to highly tissue-specific changes in the expression of genes involved in key functions of both islets and liver. To gain insights into the mechanisms of tissue-specific Hnf1alpha regulation, we integrated expression studies ...[more]

PMID: 19289501

Similar Datasets

Transcription profiling of pancreatic islets from heterozygous Hnf1a-mutant and wild type mice

Project description:Pancreatic islets were isolated from Hnf1a+/- (Hepatocyte nuclear factor 1 alpha) and wild-type mice and cultured ex vivo for two days in RPMI medium with 10% FBS before RNA extraction. The transcription profiles were obtained using Affymetrix GeneChip Mouse Genome 430 2.0 arrays [Mouse430_2].

2009-03-21 | E-MEXP-1979 | biostudies-arrayexpress

Transcription profiling of liver from Hnf1a-deficient and wild type mice

Project description:RNA was extracted from Hnf1a/Tcf1 (Hepatocyte Nuclear Factor 1 alpha) knockout and wild-type mouse liver fractions. Gene expression profiles were compared using Affymetrix GeneChip Mouse Genome 430 2.0 arrays [Mouse430_2].

2009-03-21 | E-MEXP-1709 | biostudies-arrayexpress

Transcription profiling of pancreatic islets from wild type, pancreas-specific Hnf4alpha knockout, heterozygous Hnf1alpha, and double mutant mice

Project description:Gene expression differences between wild-type, pancreas-specific Hnf4alpha knockout (Hnf4a-pKO), heterozygous Hnf1alpha (Tcf1) (Hnf1aHET), and double mutant (Hnf4a-pKO;Hnf1aHET) mouse pancreatic islets were assesed using amplified RNA samples from islets of matched quality and endocrine purity, obtained from 60-75 day-old control and genetically modified male mice after 48 hours in culture. RNA was amplified using the Affymetrix GeneChIP two-cycle protocol and hybridized to Affymetrix GeneChip Mouse Genome 430 2.0 arrays [Mouse430_2].

2010-03-01 | E-MEXP-1729 | biostudies-arrayexpress

HNF1A, UTX, H3K27me3 and H3K27ac ChIP-seq in wild-type and UTX- or HNF1A-deficient mouse pancreas

Project description:HNF1A and UTX are putative tumor suppressors in pancreatic cancer. In this study, we have combined mouse genetics, transcriptomics and genome binding studies to link HNF1A and UTX in a molecular mechanism that suppresses pancreatic cancer. In this session, we have profiled UTX, HNF1A, H3K27me3 and H3K27ac in normal and UTX- or HNF1A-deficient mouse pancreas by ChIP-seq experiments. We show that HNF1A recruits UTX to its genomic targets in pancreatic acinar cells, which results in remodeling of the chromatin landscape and activation of a broad transcriptional program of differentiated acinar cells, which in turn indirectly suppresses tumor suppressor pathways.

2019-12-20 | E-MTAB-7944 | biostudies-arrayexpress

RNA-seq of wild-type and Utx- or Hnf1a-deficient mouse pancreas

Project description:HNF1A and UTX are putative tumor suppressors in pancreatic cancer. In this study, we have combined mouse genetics, transcriptomics and genome binding studies to link HNF1A and UTX in a molecular mechanism that suppresses pancreatic cancer. In this session, we have determined the transcriptome of HNF1A and UTX in the exocrine pancreas. We show that HNF1A recruits UTX to its genomic targets in pancreatic acinar cells, which results in remodeling of the chromatin landscape and activation of a broad transcriptional program of differentiated acinar cells, which in turn indirectly suppresses tumor suppressor pathways.

2019-12-20 | E-MTAB-7945 | biostudies-arrayexpress

scRNA-seq of pancreatic islets from control and Haster-pKO mice

Project description:Pancreas specific deletion of the Haster promoter region results in a variegated phenotype in pancreatic islets with overexpression or silencing of the Hnf1a gene. To determine the transcriptional consequence of the overexpression or silencing of Hnf1a is islet cells from the Haster pKO mice (Haster loxP/loxP;Pdx1-Cre), we performed scRNA-seq of pancreatic islets from control and adult female Haster pKO mice.

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Human Pancreatic Islets Expressing HNF1A Variant Have Defective β cell Transcriptional Regulatory Networks

Project description:Using an integrated approach to characterize the pancreatic tissue and isolated islets from a 33-year-old with 17 years of type 1 diabetes (T1D), we found donor islets contained β cells without insulitis and lacked glucose-stimulated insulin secretion despite a normal insulin response to cAMP-evoked stimulation. With these unexpected findings for T1D, we sequenced the donor DNA and found a pathogenic heterozygous variant in hepatocyte nuclear factor 1 alpha (HNF1A). In one of the first studies of human pancreatic islets with a disease-causing HNF1A variant associated with the most common form of monogenic diabetes, we found that HNF1A dysfunction leads to insulin-insufficient diabetes reminiscent of T1D by impacting the regulatory processes critical for glucose-stimulated insulin secretion and suggest a rationale for a therapeutic alternative to current treatment.

2018-09-22 | GSE120299 | GEO

UMI-4C in control and HASTER-deficient EndoC-betaH3 cells overexpressing HNF1A

Project description:The HASTER promoter region is a cis-regulatory element that stabilizes the transcription HNF1A. If HASTER is deleted after beta cells have been formed and HNF1A is already stably expressed, HASTER is not required to maintain HNF1A activity, and is only required to provide negative feedback on HNF1A. HNF1A binding to the HASTER promoter mediates the repression of the HNF1A gene itself. To determine whether HNF1A binding to the HASTER promoter remodels 3D chromatin interactions of the HNF1A promoter, we performed UMI-4C experiments in wild type and HASTER-promoter KO EndoC-betaH3 cells with or without doxycycline-induced HNF1A overexpression using the HNF1A promoter as viewpoint.

2022-05-01 | E-MTAB-11473 | biostudies-arrayexpress

HNF1A deficiency impairs β-cell fate, granule maturation and function

Project description:Mutations in HNF1A cause Maturity Onset Diabetes of the Young type 3, the second most frequent form of diabetes caused by single gene mutation. We generated human pancreatic stem cell-derived endocrine cells with mutations in HNF1A and show that HNF1A deficiency impairs scβ-cell fate, insulin granule maturation and the secretion of insulin in a glucose responsive manner. Single-cell RNA sequencing reveals that HNF1A orchestrates a network of genes involved in glucose metabolism, zinc transport, calcium ion binding and hormone exocytosis. Furthermore, in both patients and stem cell-derived β-cells, HNF1A deficiency altered the stoichiometry of secreted c-peptide to insulin. Sulfonylurea, used in the treatment of these patients, restored both insulin secretion and stoichiometry. Significantly, uncoupling of c-peptide and insulin secretion as described here questions the common practice in using c-peptide as a proxy to evaluate β-cell function. We also demonstrate that correction of the HNF1A locus restores function, providing a path to cell therapy.

2019-03-16 | GSE128331 | GEO

Expression profile of HNF1A knockdown and overexpression in 22RV1 and LNCaP cells respectively

Project description:To determine genes regulated by HNF1A in 22Rv1, we performed siRNA mediated knockdown of HNF1A using pooled siHNF1A (L-008215-00-0005 5 nmol) and pooled siSCR purchased from Dharmacon. RNA was harvested 3 days after transfection and gene expression profiling was performed. Similarly to determine genes regulated by HNF1A in LNCaP, we performed retroviral transduction of LNCaP cells in duplicate for HNF1A and empty vector control expression. cDNA for HNF1A in RC211201 vector (origene) was subcloned into a murine stem cell virus (MSCV)-based retroviral vector with hygromycin selection marker (Addgene). After 3 days of transduction, cells were selected for four days in hygromycin and later on RNA was harvested for gene expression profiling.

2017-11-01 | GSE85556 | GEO

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