Aporhodopirellula sp. GIP
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ABSTRACT:
PROVIDER: PRJNA1086367 | ENA |
REPOSITORIES: ENA
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Project description:Primary cultures of Cerebellar Granule Neurons (CGNs) have been extensively utilized to examine the signal transduction mechanisms underlying neuronal apoptosis. We conducted whole-genome expression profiling to decipher the transcriptional program controlling the apoptotic/survival switch in cerebellar granule neurons (CGNs) following the induction of apoptosis by serum and potassium deprivation and their rescue by gastric inhibitory polypeptide (Gip), substance p (Sp), insulin-like growth factor-1 (Igf1) or pituitary adenylyl cyclase-activating polypeptide (Pacap). Our results reveal the transcriptional changes intersecting neuronal apoptosis and survival and form the basis for further functional analyses and pharmacological exploitation to identify neuroprotective drugs. After six days âin vitroâ (DIV), extracellular KCl of CGNs was shifted from 25 to 5 mM for neuronal apoptotic death induction. After two washes with serum-free BME containing 5 mM KCl, neurons were incubated with the same medium for 6 h (K5), while control neurons were incubated with serum free medium supplemented with 25 mM KCl (K25). K5 neurons were also treated with a maximal effective dose of Gip, Sp, Igf1 and Pacap. Four biological replicates (derived from the same litter) for each of the experimental conditions (K25, K5, K5 + Gip; K25, K5, K5 + Sp; K25, K5, K5 + Igf1; K25, K5, K5 + Pacap) were analyzed.
2016-07-03 | E-GEOD-67788 | biostudies-arrayexpress
Project description:Primary cultures of Cerebellar Granule Neurons (CGNs) have been extensively utilized to examine the signal transduction mechanisms underlying neuronal apoptosis. We conducted whole-genome expression profiling to decipher the transcriptional program controlling the apoptotic/survival switch in cerebellar granule neurons (CGNs) following the induction of apoptosis by serum and potassium deprivation and their rescue by gastric inhibitory polypeptide (Gip), substance p (Sp), insulin-like growth factor-1 (Igf1) or pituitary adenylyl cyclase-activating polypeptide (Pacap). Our results reveal the transcriptional changes intersecting neuronal apoptosis and survival and form the basis for further functional analyses and pharmacological exploitation to identify neuroprotective drugs.
2016-01-01 | GSE67788 | GEO
Project description:Erythrobacter sp. gip.4 top 5 - Genome sequencing and assembly
| PRJNA1267942 | ENA
Project description:Abstract submitted to the Journal of clinical encodcrinology and metabolism: The molecular mechanisms responsible for the ectopic expression of the GIP receptor in the adrenal cortex of patients with GIP-dependent Cushing’s syndrome (CS) are unknown. Chronic adrenal stimulation by ACTH in Cushing’s disease (CD) or by GIP in GIP-dependent AIMAH both lead to induction of a set of genes which stimulate adrenal proliferation and steroidogenesis. The objective of this study was to compare the whole genome expression profile of adrenal glands of five cases of GIP-dependent bilateral macronodular adrenal hyperplasia with CS, one case of GIP-dependent adenoma, compared to five cases of ACTH-dependant hyperplasias (CD) and a pool of adrenals from 62 normal individuals. We used the genome-spanning Affymetrix U133 plus 2.0 microarray oligochips to identify genes differentially expressed specifically in GIP-dependent CS and which would be candidate genes implicated in the ectopic expression of the GIP receptor in the adrenal cortex. After data normalization and filtering, genes with differential expression were identified with a multi-step statistical analysis involving a student’s t-test, a filter on flags and a SAM analysis. A total of 721 probesets were thus isolated with intensity levels robustly related to the presence of a GIP-dependent hyperplasia. We performed a functional classification to further define potentially important biological processes and signaling mechanism for the formation of GIP-dependent AIMAH. Various probesets were related to metabolic processes, cell-surface and intracellular signaling, tumorigenesis, transport and transcription factors. The most relevant genes had their expression profile confirmed by real-time RT-PCR. This study reports an extensive series of potentially novel targets in the identification of the molecular mechanisms of ectopic expression of the GIP-receptor in this pathology. Keywords: Comparative genomic analysis
2006-06-16 | GSE4060 | GEO
Project description:The mechanisms responsible for the ectopic adrenal expression of glucose-dependent insulinotropic peptide (GIP) receptor (GIPR) in GIP-dependent Cushing's syndrome (CS) are unknown. Chronic adrenal stimulation by ACTH in Cushing's disease or GIP in GIP-dependent ACTH-independent macronodular adrenal hyperplasia both lead to the induction of genes implicated in adrenal proliferation and steroidogenesis. OBJECTIVE: The objective of the study was to identify genes differentially expressed specifically in GIP-dependent CS that could be implicated in the ectopic expression of GIPR. METHODS: We used the Affymetrix U133 plus 2.0 microarray oligochips to compare the whole genome expression profile of adrenal tissues from five cases of GIP-dependent bilateral ACTH-independent macronodular adrenal hyperplasia with CS, one case of GIP-dependent unilateral adenoma with CS, five cases of ACTH-dependent hyperplasias, and a pool of adrenals from 62 normal individuals. RESULTS: After data normalization and statistical filtering, 723 genes with differential expression were identified, including 461 genes or sequences with a known functional implication, classified in eight dominant functional classes. Specific findings include repression of perilipin, the overexpression of 13 G protein-coupled receptors, and the potential involvement of Rho-GTPases. We also isolated 94 probe sets potentially linked to the formation of GIP-dependent nodules adjacent to the diffuse hyperplasia. These included probe sets related to the linker histone H1 and repression of RXRa and CCND2. The expression profiles for eight genes were confirmed by real-time RT-PCR. CONCLUSION: This study identified an extensive series of potentially novel target candidate genes that could be implicated in the molecular mechanisms of ectopic expression of the GIPR as well as in the multistep progression of GIP-dependent CS.
2007-10-02 | E-GEOD-4060 | biostudies-arrayexpress
Project description:Clinical investigations show that short-term treatment with gastric inhibitory polypeptide (GIP) acutely decreases serum markers of bone resorption and may increase bone formation. We report that the GIP receptor (GIPR) is expressed in human osteoclasts. Furthermore, GIP inhibits osteoclastogenesis, delays and inhibits bone resorption, and increases osteoclast apoptosis by acting upon multiple signaling pathways to impair nuclear translocation of nuclear factor of activated T cells 1 (NFATc1) and nuclear factor-κB (NFκB). Human osteoblasts also express GIPR. Although GIP improves osteoblast survival via cAMP and Akt-mediated pathways, expression of osteoblast-specific genes including RUNX2 and BGLAP and bone formation is not changed by GIP. Treatment of co-cultures of osteoclasts and osteoblasts with GIP decreased bone resorption but did not change formation. Antagonizing the GIPR with GIP(3-30)NH2 abolished the effects of GIP on osteoblasts and osteoclasts. Clinical studies are needed to determine if longer-term GIPR activation uncouples bone resorption and formation and improves bone mass
2022-10-01 | GSE201100 | GEO
Project description:The intention of this clinical study was to investigate the effect of GIP administration for 240 min on gene expression in human subcutaneous adipose tissue. Three conditions have been tersted: 1. Sole infusion of GIP or NaCl as control; 2. GIP or NaCl administration under euglycemic-hyperinsulinemic clamp conditions; 3. GIP or NaCl administration under hyperglycemic-hyperinsulinemic clamp conditions to mimic the postprandial state.
2012-09-05 | GSE40589 | GEO
Project description:The intention of this clinical study was to investigate the effect of GIP administration for 240 min on gene expression in human subcutaneous adipose tissue. Three conditions have been tersted: 1. Sole infusion of GIP or NaCl as control; 2. GIP or NaCl administration under euglycemic-hyperinsulinemic clamp conditions; 3. GIP or NaCl administration under hyperglycemic-hyperinsulinemic clamp conditions to mimic the postprandial state. In each participant a complete physical examination and evaluation of medical history was performed, including an oral glucose tolerance test (oGTT) with 75 g glucose after overnight fast to ensure the metabolic state. Standard fasting laboratory and clinical chemistry evaluations were done. Synthetic human GIP (1-42) was dissolved in saline (0.9% NaCl-solution) under sterile conditions. All studies were done in the morning in the overnight fasted state (>10h since last meal). The effect of GIP administration on gene expression in subcutaneous adipose tissue was studied under 3 different conditions in a single blind design. Either the participants received only a GIP- or a saline- infusion (0.9% NaCl-isotonic solution, Fresenius, Germany) for 240 min. At different investigation days participants underwent euglycemic (EU)- and hyperglycemic (HC), hyperinsulinemic clamps combined with GIP- or placebo-infusions for 240 min at different examination days in a randomized, single-blind, crossover design. The capillary glucose concentration was 80mg/dl during EU-clamp and 140mg/dl during HC-clamp. The following numbers of treatments were performed: EU with GIP-infusion (N=9); EU with NaCl-infusion (N=9); HC with GIP-infusion (N=8), HC with NaCl-infusion (N=8); sole GIP-infusion (N=11) and sole placebo-infusion (N=11). Between examination days an intermission time of at least 7 days was maintained.
2012-09-05 | E-GEOD-40589 | biostudies-arrayexpress
Project description:Immune-mediated beta cell destruction and lack of alpha cell responsiveness to hypoglycaemia are hallmarks of type 1 diabetes pathology. The incretin hormone glucose-dependent insulinotropic polypeptide (GIP) may hold therapeutic potential for type 1 diabetes due to its insulinotropic and glucagonotropic effects as well as its beta cell protective effects shown in rodent islets. Here, we examined the functional and transcriptomic effects of GIP treatment upon diabetogenic cytokine exposure to interleukin (IL)-1β ± interferon (IFN)-γ in human EndoC-βH5 beta cells and isolated human islets, respectively. GIP dose-dependently augmented glucose-stimulated insulin secretion from EndoC-βH5 cells and increased insulin and glucagon secretion from human islets during high and low glucose concentrations, respectively. The insulinotropic effect of GIP in EndoC-βH5 cells was abrogated by KN-93, an inhibitor of calcium/calmodulin-dependent protein kinase 2 (CaMK2). GIP did not prevent cytokine-induced apoptosis or cytokine-induced functional impairment of human EndoC-βH5 cells. GIP also did not prevent cytokine-induced apoptosis in human islets. GIP treatment of human islets with or without cytokines for 24 hours did not significantly impact the transcriptome. GIP potentiated cytokine-induced secretion of IL-10 and c-c motif chemokine ligand (CCL)-2 from human islets while decreasing the secretion of c-x-c motif chemokine ligand (CXCL)-8. In EndoC-βH5 cells, GIP reduced IFN-γ-induced secretion of tumor necrosis factor (TNF)-α, IL-2, IL-6, and IL-10, but increased the secretion of CXCL8, CCL2, CCL4, and CCL11. In conclusion, our results suggest that the insulinotropic effect of GIP is CaMK2-dependent. Furthermore, our results indicate that GIP does not provide substantial cytoprotective effects against diabetogenic cytokine challenge or significantly modulate the transcriptome of human islets when applied at a supraphysiological level. GIP may, however, still exert selective inflammation-modulatory effects upon diabetogenic cytokine exposure.
2025-03-26 | GSE269993 | GEO