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Genome-wide time series analysis of gastrin induced gene expression in AR42J cells with and without protein synthesis

ABSTRACT: Genome-wide gene expression time series experiments are an important approach to studying a cells response to a given stimulus, as they enable capturing of the dynamics of the response. Moreover, information about the dynamics of the system is an important prerequisite for inferences on interactions between its components. We have performed extensive microarray-based genome-wide gene expression analyses up to 14h of the response to gastrin in AR42J adenocarcinoma cells. The gastrin reponse was also investigated in presence of the protein translation inhibitor cycloheximide. The rat cell line AR42J derived from pancreatic duct has the feature of pluripotency of the precursor cells of the gut endoderm. Furthermore, AR42J cells express gastrin receptors endogenously and are therefore frequently used as a model system to study gastrin responses. The hormone gastrin is the central regulator of gastric acid secretion and in addition plays a prominent role in regulation of growth and differentiation of gastric and colonic mucosa. Hypergastrinaemia has been linked to development of neuroendocrine gastrointestinal tumours (NE-GI) and, in conjugation with additional factors such as inflammation, to development of gastric adenocarcinoma (GA)

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE32869 | GEO | 2011/10/17

SECONDARY ACCESSION(S): PRJNA146557

REPOSITORIES: GEO

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Genome-wide time series analysis of gastrin induced gene expression in AR42J cells with and without protein synthesis

Project description:Genome-wide gene expression time series experiments are an important approach to studying a cells response to a given stimulus, as they enable capturing of the dynamics of the response. Moreover, information about the dynamics of the system is an important prerequisite for inferences on interactions between its components. We have performed extensive microarray-based genome-wide gene expression analyses up to 14h of the response to gastrin in AR42J adenocarcinoma cells. The gastrin reponse was also investigated in presence of the protein translation inhibitor cycloheximide. The rat cell line AR42J derived from pancreatic duct has the feature of pluripotency of the precursor cells of the gut endoderm. Furthermore, AR42J cells express gastrin receptors endogenously and are therefore frequently used as a model system to study gastrin responses. The hormone gastrin is the central regulator of gastric acid secretion and in addition plays a prominent role in regulation of growth and differentiation of gastric and colonic mucosa. Hypergastrinaemia has been linked to development of neuroendocrine gastrointestinal tumours (NE-GI) and, in conjugation with additional factors such as inflammation, to development of gastric adenocarcinoma (GA) Times series up to 14h treated with gastrin, gastrin and cycloheximide, cycloheximide and control at individual timepoints

2011-10-16 | E-GEOD-32869 | biostudies-arrayexpress

Transcription profiling of rat AR42J cells treated with gastrin at multiple time points

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2010-01-01 | E-MTAB-123 | biostudies-arrayexpress

Fundic mucosa gene expression in the presence/absence of gastrin and in gastrin-CCK double knockout mice.

Project description:Fundic mucosa gene expression in wildtype vs gastrin knockout, gastrin replaced gastrin KO and gastrin-CCK double knockout mice Fundic mucosal scraping RNA were isolated from WT, Gastrin Knockout, Gastrin replaced KO and Gastrin-CCK double knockout mice. Targets from three biological replicates of each were generated and the expression profiles were determined using Affymetrix murine 430A arrays. Comparisons between the sample groups allow the identification of genes with gastrin responsiveness and Gastrin-CCK double effect . Keywords: repeat

2007-05-03 | GSE4810 | GEO

Gastrin, PAI-1 and mucosal growth. Whole organism studies in transgenic mice.

Project description:We are studying the role of PAI-1 in hypergastrinemic transgenic mice (PAI-1 knockout, HK-ATPase beta knockout and corresponding control strains). As a model of hypergastrinaemia, HK-ATPase beta knockout mice are preferred instead of giving a high dose of proton pump inhibitors daily. We have successfully crossed these two strains and generated double knockout mice (PAI-1--/HK-ATPase--) and 3 different control groups (PAI-1++/HK-ATPase++, PAI-1--/HK-ATPase++ and PAI-1++/HK-ATPase--) (9 animals in each group). The gastric phenotype of all mice has been examined by morphologic and molecular analysis after 12 months. Gastric biopsies and blood samples have been taken for histology, large scale gene expression analysis, verification of mRNA and protein expression and gastrin measurements. Global gene expression analysis has been done on gastric mucosal samples from all groups of mice. The differences between wild type mice and the transgenic animals are expected to provide novel hypotheses on the role of PAI-1 in gastrin-induced changes in the gastric mucosa.

2016-02-01 | E-MTAB-3853 | biostudies-arrayexpress

Transcription profiling of mouse fundic mucosa in the presence/absence of gastrin and in gastrin-CCK double knockout mice

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2008-06-13 | E-GEOD-4810 | biostudies-arrayexpress

Effects of a gastrin receptor antagonist (NTZ, previously named YF) on the gastric corpus mucosa of HKATPase betasubunit knockout (KO) mice

Project description:Purpose: the effects of a gastrin receptor antagonist has been studies in patients with gastrin neuroendocrine (NE) tumours due to hypergastrinemia. This mouse model of hypergastrinemia is a model for studying long term acid inhibition, including NE hyperplasia and formation of Spasmolytic polypeptide expressing metaplasia (SPEM), a proposed premalignant alteration of the stomach. Methods: RNA was isolated from the oxyntic mucosa. RNA was sequenced using standard Illumina protocols on a NextSeq 500 instrument. Results: NTZ reduced oxyntic mucosal hypertropohy and stomach weight. Neuroendocrine cell hyperplasia and NE markers were also reduced. Spasmolytic polypeptide expressing metaplasia (SPEM) was expressed in KO mice and was not affected by the gastrin receptor antagonist. Conclusions: The gastrin receptor antagonist YF reduced gastric corpus mucosal hypertrophy and NE cell hyperplasia in HKATPase KO mice, but did not affect SPEM or SPEM related genes.

2019-12-23 | GSE142513 | GEO

Transcription profiling of parietal cells isolated from WT and Gastrin Knockout mice to identify genes responsive to gastrin.

Project description:Parietal cells were isolated from WT and Gastrin Knockout mice. Targets from three biological replicates of each were generated and the expression profiles were determined using Affymetrix murine U74Av2 arrays. Comparisons between the sample groups allow the identification of genes with gastrin responsiveness. Experiment Overall Design: 3 WT parietal cell and 3 Gastrin Kncokout parietal cell replicates were analyzed

2007-08-31 | E-GEOD-2772 | biostudies-arrayexpress

Parietal cell gene expression in the presence and absence of gastrin

2005-11-15 | GSE2772 | GEO

Two Center Study to Determine Effect of G17DT on Plasma Gastrin Levels in Patients With Colorectal Cancer.

Project description:Pancreatic, gastric, and colorectal cancers have all been shown to overexpress the gastrin gene and to be sensitive to the trophic effects of the gastrin in animal models. The hypothesis of this study is that G17DT will elicit specific and high-affinity antibodies that will bind gastrin-17, thus preventing the trophic activity of cancer cells.

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Sleeve Gastrectomy Reveals the Plasticity of the Human Gastric Epithelium

Project description:Gastric acidity is essential for the function of the human stomach. pH homeostasis is facilitated by gastrin, a hormone secreted from the gastric antrum in response to a rise in pH, leading to acid secretion from the gastric corpus. Sleeve gastrectomy (SG), a bariatric surgery in which 80% of the gastric corpus is excised, presents a challenge for gastric pH homeostasis. We used histology and single-cell RNA sequencing to study the gastric antrum and corpus epithelium of naïve patients, and of patients who underwent SG years earlier. SG was associated with an increase in a sub-population of acid-secreting parietal cells which overexpress respiratory enzymes and carbonic anhydrase, and an increase in the fraction of histamine-secreting enterochromaffin-like cells (ECLs). Notably, ECLs of SG-operated patients over-expressed genes coding for biosynthesis of neuropeptides and of serotonin. Mathematical modeling of pH homeostasis by gastrin showed that fasting pH is not sensitive to nearly all model parameters. Robustness is a result of the ability of gastrin to induce acid secretion as well as increase the number of ECLs and parietal cells, a feedback analogous to a non-linear proportional and integral feedback control, that drives adaptation of the epithelium to acid-secretion demand. Quantitative predictions of the model on the gastric response to SG were validated in patients: SG induced a 5-fold increase in blood gastrin levels as early as one day post-surgery, and an over 30% increase in the number of parietal cells and ECLs per gland years after surgery. Together, these empirical and modeling data demonstrate how the human gastric epithelium remodels following SG at the molecular and cellular levels, and more generally how trophic hormones such as gastrin enable robust adaptation of tissue function to meet physiological demand.

2024-12-15 | GSE263018 | GEO

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