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A Potential Role of the Unfolded Protein Response in the Impaired Production and Release of Epinephrine in Recurrent Hypoglycemia

ABSTRACT: In order to gain further insight into the molecular mechanism(s) mediating the blunted epinephrine responses following recurrent hypoglycemia we utilized global gene expression profiling approach. Our results indicate the association between defective counterregulation (impaired epinephrine release) and the activation of the unfolded protein response as well as increased neuropeptide signaling, altered ion homeostasis and downregulation of proteins involved in Ca2+-dependent exocytosis of secretory vesicles. We compared the entire transcriptomes during recurrent (defective CRR model, 2RH) and acute hypoglycemia (normal CRR group, 2RS) in the adrenal medulla of normal Sprague-Dawley rats.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Bistra Nankova

PROVIDER: E-GEOD-82145 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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A Potential Role of the Unfolded Protein Response in the Impaired Production and Release of Epinephrine in Recurrent Hypoglycemia

Project description:In order to gain further insight into the molecular mechanism(s) mediating the blunted epinephrine responses following recurrent hypoglycemia we utilized global gene expression profiling approach. Our results indicate the association between defective counterregulation (impaired epinephrine release) and the activation of the unfolded protein response as well as increased neuropeptide signaling, altered ion homeostasis and downregulation of proteins involved in Ca2+-dependent exocytosis of secretory vesicles.

2016-07-01 | GSE82145 | GEO

Analysis of the Aedes aegypti transcriptome during flavivirus infection

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2013-03-31 | E-GEOD-28208 | biostudies-arrayexpress

Liver-dependent lung remodeling in the wake of systemic inflammation shapes responses to secondary infection

Project description::Systemic duress, like that elicited by sepsis, burns or trauma, predispose patients to nosocomial pneumonia, demanding better understanding of host pathways influencing this deleterious connection. These pre-existing circumstances are capable of triggering the hepatic acute phase response (APR), which we previously demonstrated is essential for limiting susceptibility to secondary lung infections. To identify potential mechanisms underlying protection afforded by the lung-liver axis, our studies aimed to evaluate liver-dependent lung reprogramming when a systemic inflammatory challenge precedes pneumonia. WT mice and APR-deficient littermates lacking hepatocyte STAT3 (hepSTAT3-/-), a transcription factor necessary for full APR initiation, were challenged intraperitoneally with LPS to induce endotoxemia. After 18h, pneumonia was induced by intratracheal E. coli instillation. Endotoxemia elicited significant transcriptional alterations in the lungs of WT and hepSTAT3-/- mice, with nearly 2,000 differentially expressed genes between genotypes. The gene signatures revealed exaggerated immune activity in the lungs of hepSTAT3-/- mice, which were compromised in their capacity to launch additional cytokine responses to secondary infection. Proteomics revealed substantial liver-dependent modifications in the airspaces of pneumonic mice, implicating a network of dispatched liver-derived mediators influencing lung homeostasis. These results indicate that following systemic inflammation, liver acute phase changes dramatically remodel the lungs, resulting in a modified landscape for any stimuli encountered thereafter. Based on the established vulnerability of hepSTAT3-/- mice to secondary lung infections, we believe that intact liver function is critical for maintaining the immunological responsiveness of the lungs. Further studies are needed to confirm whether and how such lung changes directly influence pneumonia susceptibility.

2021-07-23 | PXD024663 | Pride

Gut microbiome metabolites alter genomic networks in PC12 cells relevant to autism spectrum diorders

Project description:Alterations in the composition of the gut microbiome have an emerging role in brain function and behaviour. We have porposed that short chain fatty acids (SCFA) including propionate and butyrate which are present in the diet and are fermantation products of many gastrointestinal bacteria are contributing environmental factors in autism spectrum disorders (ASD). Here we used the microarray technology to compare global changes in gene expression profiles following exposure of PC12 cells to structurally related SCFA propionate and butyrate each in two different concentrations. Large number of affected genes, common for both SCFA were identified, including genetic networks and GO processes implicated in ASD. PC12 cells were exposed to propionate or butyrate. RNA was isolated from each experimental group (n=6, pooled samples) and subjected to genome-wide expression profiling using Affymetrix microarrays to reveal dose- and SCFA-specific changes in gene expression and specific molecular pathways or processes affected as compared to vehicle treated controls.

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Transcription profiling of rat adrenal medulla and PC12 cell culture to investigate genetic networks regulated by short chain fatty acids

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Gene expression profile at single nuclei level of brain tissues from diabetic mice exposed to acute or recurrent hypoglycemia.

Project description:The brain is an important controller of glucose homeostasis and mediates counterregulatory responses to hypoglycemia. We used single-nuclei transcriptomics to study the mechanisms of defective hypoglycaemia counter-regulation in brain in a model of diabetic mice exposed to acute or recurrent hypoglycemia.

2023-10-02 | GSE226277 | GEO

MicroRNA-7a overexpression in VMH restores the sympathoadrenal response to hypoglycemia

Project description:It is proposed that the impaired sympathoadrenal response to hypoglycemia induced by recurrent insulin-induced hypoglycemia (RH) is an adaptive phenomenon induced by specific changes in microRNA expression in the ventromedial hypothalamus (VMH). To test this hypothesis, genome-wide microRNAomic profiling of the VMH by RNA-sequencing was performed in control and RH treated rats. Differential expression analysis identified microRNA-7a-5p and microRNA-665 as potential mediators of this phenomenon. To further test this hypothesis, experiments were conducted consisting of targeted lentiviral-mediated overexpression of microRNA-7a-5p and downregulation of microRNA-665 in the VMH. Hyperinsulinemic hypoglycemic clamp experiments demonstrated that targeted overexpression of microRNA-7a-5p (but not downregulation of microRNA-665) in the VMH of RH rats restored the epinephrine response to hypoglycemia. This restored response to hypoglycemia was associated with a restoration of GABAA receptor gene expression. Finally, a direct interaction of microRNA-7a-5p with 3’-UTR of GABAA receptor α1-subunit (Gabra1) gene was demonstrated in a luciferase assay. These findings indicate that 1) the impaired sympathoadrenal response induced by RH is associated with changes in VMH microRNA expression, and 2) microRNA-7a-5p, possibly via direct downregulation of GABA receptor gene expression, may serve as a mediator of the altered sympathoadrenal response to hypoglycemia.

2019-10-17 | GSE138472 | GEO

Preimplantation Factor Effect on Endometrial and Decidual Cells

Project description:Embryos secrete preimplantation factor (PIF), a peptide present in maternal circulation during viable pregnancy. We compared downstream synthetic PIF effect on gene expression in non-pregnant Human Endometrial Stromal Cell (HESC) and First Trimester Decidual cell (FTDC) culture to mimic the maternal intrauterine environment during embryo implantation and trophoblast invasion. Cells were cultured in triplicate with and without synthetic PIF for 24 hours. Cultured cells were then pooled for chip analysis. Altered gene expression relative to controls was assessed by Affymetrix microarray

2013-06-21 | E-GEOD-46326 | biostudies-arrayexpress

Rattus norvegicus

Project description:A Potential Role of the Unfolded Protein Response in the Impaired Production and Release of Epinephrine in Recurrent Hypoglycemia

| PRJNA324140 | ENA

Expression data from liver, PFC and amygdala of mice treated with PPAR agonists

Project description:Peroxisome proliferator-activated receptors (PPARs) are nuclear hormone receptors that act as ligand-activated transcription factors. Although prescribed for dyslipidemia and type-II diabetes, PPAR agonists have demonstrated therapeutic properties for several brain disorders, including alcohol dependence. PPAR agonists decrease ethanol consumption and reduce withdrawal severity and susceptibility to stress-induced relapse in rodents. However, the cellular and molecular mechanisms facilitating these properties have yet to be investigated and little is known about their effects in the brain. We tested three PPAR agonists in a continuous access two-bottle choice (2BC) drinking paradigm and found that tesaglitazar and fenofibrate decreased ethanol consumption in male C57BL/6J mice while bezafibrate did not. Hypothesizing that fenofibrate and tesaglitazar are causing brain gene expression changes that precipitate the reduction in ethanol drinking, we gave daily oral injections of fenofibrate, tesaglitazar and bezafibrate to mice for eight consecutive days and collected liver, prefrontal cortex and amygdala 24 hours after last injection. RNA was isolated and purified using MagMAX-96 Total RNA Isolation Kit. Biotinylated, amplified cRNA was generated using Illumina TotalPrep RNA Amplification Kit and hybridized to Illumina MouseWG-6 v2.0 Expression microarrays. Mice were divided into four groups (N=10 per group): fenofibrate, tesaglitazar, bezafibrate and saline. See summary and protocols for details.

2015-04-14 | E-GEOD-67796 | biostudies-arrayexpress

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