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Integrated molecular landscape perturbations underlie cellular responses during hyperammonemia

ABSTRACT: Integrated molecular landscape perturbations underlie cellular responses during hyperammonemia

PROVIDER: PRJNA720399 | ENA |

REPOSITORIES: ENA

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Integrated molecular landscape perturbations underlie cellular responses during hyperammonemia [ATAC-seq]

Project description:Integrated molecular landscape perturbations underlie cellular responses during hyperammonemia [ATAC-seq]

| PRJNA720401 | ENA

Integrated molecular landscape perturbations underlie cellular responses during hyperammonemia [human RNA-seq]

Project description:Integrated molecular landscape perturbations underlie cellular responses during hyperammonemia [human RNA-seq]

| PRJNA720402 | ENA

Integrated molecular landscape perturbations underlie cellular responses during hyperammonemia [mouse RNA-seq]

Project description:Integrated molecular landscape perturbations underlie cellular responses during hyperammonemia [mouse RNA-seq]

| PRJNA720403 | ENA

Integrated molecular landscape perturbations underlie cellular responses during hyperammonemia [ATAC-seq]

Project description:Ammonia is a cytotoxic molecule generated during cellular functions and by the gut microbiome. Dysregulated ammonia metabolism initiates a hyperammonemic stress response (HASR). Hyperammonemia occurs in many chronic diseases but there is limited understanding of the overall consequences of HASR. A comprehensive array of unbiased approaches was used to identify global responses during hyperammonemia with experimental validation of critical findings. Protein/gene expression and chromatin accessibility in hyperammonemic murine myotubes and mouse skeletal muscle tissue were analyzed by quantitative proteomics, RNA sequencing (RNAseq), and Assay for Transposase Accessible Chromatin Sequencing (ATACseq). Unique clusters of expression/accessibility changes were identified in hyperammonemic myotubes. In hyperammonemic mouse muscle and myotubes, we identified enrichment of pathways involved in oxidative phosphorylation, calcium signaling, hypoxia inducible factor-1, and apoptosis and regulation of protein synthesis were altered during HASR and were experimentally validated. Enrichment of senescence signaling and glycosylation pathways during HASR were novel observations. Comparisons with RNAseq data from skeletal muscle from human patients with cirrhosis revealed similar perturbations, demonstrating the translational relevance of our observations. We identified several novel regulatory pathways during HASR that are conserved in different models and across species, and whose dysregulation could significantly impact skeletal muscle structure and function.

2021-07-28 | GSE171642 | GEO

Integrated molecular landscape perturbations underlie cellular responses during hyperammonemia

2021-07-27 | PXD025321 | Pride

Integrated molecular landscape perturbations underlie cellular responses during hyperammonemia [mouse RNA-seq]

2021-07-28 | GSE171644 | GEO

Integrated molecular landscape perturbations underlie cellular responses during hyperammonemia [human RNA-seq]

2021-07-28 | GSE171643 | GEO

Integrated molecular landscape perturbations underlie cellular responses during hyperammonemia

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-07-27 | GSE171645 | GEO

Integrated multiomics analysis identifies molecular landscape perturbations during hyperammonemia in skeletal muscle and myotubes.

Project description: Not available

| S-EPMC8424232 | biostudies-literature

Glutaminase 2 Knockdown Reduces Hyperammonemia and Associated Lethality of Urea Cycle Disorder Mouse Model

Project description:Urea cycle disorders with hyperammonemia remain difficult to treat and eventually necessitate liver transplantation. An ornithine transcarbamylase defect (Otcspf-ash) mouse model, a model of urea cycle disorder, was used to test whether knockdown of a key glutamine metabolism enzyme glutaminase 2 (Gls2) or glutamine dehydrogenase 1 (Glud1) could rescue the hyperammonemia and associated lethality induced by a high protein diet. Reduced hepatic expression of Gls2, but not Glud1, by AAV8-mediated delivery of a short hairpin RNA in Otcspf-ash mice diminished hyperammonemia, reduced body weight loss, and reduced lethality. These data suggest that Gls2 hepatic knockdown could help alleviate risk for hyperammonemia and other clinical manifestations of patients suffering from defects in the urea cycle.

2022-06-07 | GSE179342 | GEO

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