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ABSTRACT: HZRG-MCD

PROVIDER: PRJNA799458 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17703728.fastq.gz	Fastqsanger.gz
	SRR17703729.fastq.gz	Fastqsanger.gz
	SRR17703730.fastq.gz	Fastqsanger.gz
	SRR17703731.fastq.gz	Fastqsanger.gz
	SRR17703732.fastq.gz	Fastqsanger.gz

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Difference of microRNA expressions between a mouse model of NASH(MCD diet) and normal mouse.

Project description:The microRNAs expression was markedly altered with the MCD diet. Using a custom microarray platform, we analyzed the expression levels of 1135 mouse microRNA probes in liver tissue that were fed MCD diet.

2015-03-01 | E-GEOD-55593 | biostudies-arrayexpress

Comparison of Glomerular Transcriptome Profiles of Adult-Onset Steroid Sensitive Focal Segmental Glomerulosclerosis and Minimal Change Disease

Project description:To search for biomarkers to differentiate Adult-Onset Steroid Sensitive focal segmental glomerulosclerosis (FSGS) and minimal change disease (MCD). Compared the profiles of glomerular transcriptomes between patients with FSGS and patients with MCD using microarray analysis. This dataset is part of the TransQST collection.

2017-01-04 | E-GEOD-69814 | biostudies-arrayexpress

Single Cell Gene Expression Profiling of CD45+ Cells in Mouse Liver with or without Empagliflozin (EMPA) Treatment

Project description:Single-Cell Sequencing Reveals Immune Cell Subtype Differences in Mouse Liver Between MCD and MCD+Empagliflozin (EMPA) Treatment.

2024-10-01 | GSE271786 | GEO

Difference of microRNA expressions between a mouse model of NASH(MCD diet) and normal mouse.

Project description:The microRNAs expression was markedly altered with the MCD diet.

2015-03-01 | GSE55593 | GEO

Effect of methionine-chorine-deficient diet (MCD) on microRNA expression in murine liver [miRNA]

Project description:It is known that administration of MCD induces a severe state of hepatic fibrosis in mice. Recently, many microRNAs (miRNAs) with pro- or anti-fibrotic properties have been identified during hepatic fibrosis. To attempt to elucidate molecular mechanism of hepatic fibrosis involved in miRNA fnction, we performed comprehensive analysis of miRNA expression by microarray using RNAs prepared from liver of wild-type mice fed with normal diet (ND) or MCD.

2023-12-06 | GSE249486 | GEO

A deletion in Eml1 leads to bilateral subcortical heterotopia in the tish rat

Project description:Malformations of cortical development (MCD) are present in up to 40% of children with pharmacoresistant epilepsy. Although epilepsy surgery can be successful in a subset of children, not all forms of MCD are operable. Understanding the genetic and neurobiological mechanisms underlying MCD and MCD-related epilepsy are necessary for the development of novel anti-epilepsy drugs. The tish (telencephalic internal structural heterotopia) rat is a unique model of MCD and spontaneous seizures, but the underlying genetic mutation has been, heretofore, unknown. DNA and RNA-sequencing revealed that a deletion encompassing a previously unannotated exon markedly diminished EML1 transcript and protein abundance in the tish brain. Developmental electrographic characterization of the tish rat demonstrated spontaneous spike-wave discharge (SWD) bursts beginning as early as postnatal day (P) 17. A dihybrid cross demonstrated that the mutantEml1 allele segregates with the observed dysplastic cortex and SWD bursts in monogenic autosomal recessive frequencies. Our data link the development of the bilateral, heterotopic dysplastic cortex of the tish rat to a mutation in Eml1 and provide a novel rat model of MCD.

2020-03-28 | GSE147663 | GEO

Methionine and choline deficiency rewires transcriptional programs to recapitulate molecular features of human MASH

Project description:Metabolic dysfunction-associated steatohepatitis (MASH) is a leading cause of cirrhosis and liver related mortality, but it remains unclear how nutrient stresses drive coordinated transcriptional remodeling in the pathogenesis of MASH. Clinical studies reported that methionine and choline deficiency (MCD) promotes chronic liver diseases. Multiple types of MCD diets have been adopted to establish MASH mouse models. However, how methionine and choline deficiency modulates cell-intrinsic transcriptional responses across parenchymal and nonparenchymal liver cell types, and whether these effects recapitulate human MASH, remains unclear. Here, we generated a customized MCD cell culture medium to induce nutrient stress in HepG2 cells, endothelial cells, bone marrow derived macrophages, and hepatic stellate cells (HSCs). RNA sequencing was performed to characterize transcriptional regulations in response to MCD. Across cell types, lack of methionine and choline induced transcriptional program of inflammatory and stress response and suppressed metabolic pathways and cell-cycle progression, suggesting a proliferation pause as a compensatory stress-adaptive response that preserves cell viability and essential functions. In addition to these shared responses, MCD stress also caused distinct cell type-specific outputs that could contribute to the pathogenesis of MASH. Integrated analysis of these datasets with human MASH liver single nucleus transcriptomic data demonstrated that MCD condition recapitulates multiple pathophysiological features of human MASH, including the elevated inflammation, enhanced hepatocyte death, disrupted redox balance, altered metabolic homeostasis, and HSC activation. These findings not only uncover how MCD stress promotes MASH progression, but also provide a conceptual basis to guide future use of MCD diet-induced models in MASH studies.

2026-03-25 | GSE319635 | GEO

RNA-seq data from mice liver fed with MCD

Project description:We fed control mice and Slc7a11-LTG mice methionine and Choline Deficient (MCD) to induce NASH. Whole-genome RNA sequencing were then performed in the livers of control and LTG mice fed with MCD.

2025-09-09 | GSE213182 | GEO

Transcription profiling by array to identify the effects of n-3 polyunsaturated fatty acids on non-alcoholic steatohepatitis in mice

Project description:The pathogenesis of non-alcoholic fatty liver disease (NAFLD) is associated with abnormalities of liver lipid metabolism, especially with the accumulation of saturated fatty acids (FA). On the contrary, a diet enriched with n-3 polyunsaturated FA (n-3-PUFA) has been reported to ameliorate the progression of NAFLD. The aim of our study was to investigate the impact of dietary n-3-PUFA enrichment on the development of NAFLD and liver lipidome. Mice were fed for 6 weeks either high-fat methionine choline-deficient diet (MCD) or standard chow (two groups fed MCD, two control groups, both with or without n-3-PUFA). Genome-wide transcriptome analysis of liver tissue was performed and revealed differences in liver mRNA transcriptomes after MCD as well as n-3-PUFA administration.

2023-12-14 | E-MTAB-13399 | biostudies-arrayexpress

Anti-nephrin autoantibodies in minimal change disease and focal segmental glomerulosclerosis (proteomics)

Project description:Background: Minimal change disease (MCD) and focal-segmental glomerulosclerosis (FSGS) are immune-mediated glomerular diseases manifesting as nephrotic syndrome. Autoantibodies against the podocyte slit diaphragm protein nephrin were recently identified in a subset of patients with minimal change disease, but their clinical and pathophysiological significance is largely unknown. Methods: Using immunoprecipitation assays, we performed a blinded screening for anti-nephrin antibodies in diagnostic and follow-up serum samples from adult patients with biopsy-proven MCD, FSGS, IgA nephropathy, and membranous nephropathy in comparison to healthy controls in two independent patient cohorts from Hamburg, Germany, and Bari, Italy. We further established a mouse model of anti-nephrin antibody-induced disease by active immunization using the recombinant murine nephrin ectodomain. Results: Anti-nephrin autoantibodies were detected in 50 of 110 (45%) patients with MCD, 8 of 107 (7%) patients with FSGS, 1 of 50 (2%) patients with membranous nephropathy, 0 of 48 (0%) patients with IgA nephropathy, and 0 of 67 (0%) healthy individuals. During follow-up, presence, and absence of anti-nephrin autoantibodies in patients with MCD and FSGS strongly correlated with active disease and remission, respectively. Immunization of mice induced anti-nephrin autoantibody formation and a highly dynamic phenotype with severe nephrotic syndrome and the histological features of MCD. Mechanistically, anti-nephrin autoantibodies induced nephrin phosphorylation at Tyr1191, cytoskeletal rearrangement, and downregulation of key podocyte proteins. Conclusion: Anti-nephrin antibodies are a valuable biomarker of disease activity in patients with MCD and FSGS, and binding of anti-nephrin antibodies at the podocyte slit diaphragm induces MCD with nephrotic syndrome.

2024-05-27 | PXD047417 | Pride

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