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Transcriptomic characterization of control and drug-treated APOB-mutant organoids to study steatosis-resolving drug effects

ABSTRACT: Transcriptomic characterization of control and drug-treated APOB-mutant organoids to study steatosis-resolving drug effects

PROVIDER: PRJNA915399 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22882355_1.fastq.gz	Fastqsanger.gz
	SRR22882355_2.fastq.gz	Fastqsanger.gz
	SRR22882356_1.fastq.gz	Fastqsanger.gz
	SRR22882356_2.fastq.gz	Fastqsanger.gz
	SRR22882357_1.fastq.gz	Fastqsanger.gz

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Transcriptomic characterization of control and drug-treated APOB-mutant organoids to study steatosis-resolving drug effects

Project description:We treated APOB-mutant organoids with different anti-NAFLD drug candidates that were effective at resolving steatosis. To understand the mechanisms of drug action and adverse drug effects we performed bulk RNA-sequencing on drug-treated and vehicle-treated APOB mutant organoids.

2023-02-23 | GSE221705 | GEO

Identification of dysregulated transcripts in apob-1(RNAi);apob-2(RNAi) planarians

Project description:ApoB-1 and ApoB-2 are intestine-enriched regulators of lipoprotein secretion in planarians. The goal of this study was to identify differentially expressed transcripts in uninjured apob-1(RNAi);apob-2(RNAi) double knockdown planarians relative to egfp(RNAi) control animals.

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Identification of dysregulated transcripts in apob-1(RNAi) apob-2(RNAi) planarians

Project description:Identification of dysregulated transcripts in apob-1(RNAi) apob-2(RNAi) planarians

| PRJNA728883 | ENA

Metabolic Drug Response Phenotyping in Colorectal Cancer Organoids by LC-QTOF-MS

Project description:As metabolic rewiring is crucial for cancer cell proliferation, metabolic phenotyping of patient-derived organoids is desirable to identify drug-induced changes and trace metabolic vulnerabilities of tumor subtypes. We established a novel protocol for metabolomic and lipidomic profiling of colorectal cancer organoids by LC-QTOF-MS facing the challenge of capturing metabolic information from minimal sample amount (< 500 cells/injection) in the presence of extracellular matrix (ECM). The best procedure of the tested protocols included ultrasonic metabolite extraction with acetonitrile/methanol/water (2:2:1, v/v/v) without ECM removal. To eliminate ECM-derived background signals, we implemented a data filtering procedure based on p-value and fold change cut-offs which retained features with signal intensities >120% compared to matrix-derived signals present in blank samples. As a proof-of-concept, the method was applied to examine the early metabolic response of colorectal cancer organoids to 5-fluorouracil treatment. Statistical analysis revealed dose-dependent changes in the metabolic profiles of treated organoids including elevated levels of 2'-deoxyuridine, 2'-O-methylcytidin, inosine and 1-methyladenosine and depletion of 2'-deoxyadenosine and specific phospholipids. In accordance with the mechanism of action of 5-fluorouracil, changed metabolites are mainly involved in purine and pyrimidine metabolism. The novel protocol provides a first basis for the assessment of metabolic drug response phenotypes in 3D organoid models.

2021-10-12 | MTBLS2130 | MetaboLights

Retinal organoids provide a suitable tool for toxicological drug screening – a comprehensive study validating well-known drug effects on retinal organoids

Project description:Drug toxicity screening on retina is essential for the development of safe therapies for a large number of diseases, whilst preserving visual acuity and function. To this end, retinal organoids derived from human pluripotent stem cells (hPSCs) provide a suitable screening platform due to their similarity to human retina and the ease of generation in large-scale formats, offering almost unlimited excess of tissue. Two hPSC cell lines were differrentiated to retinal organoids which comprised all key retinal cell types in multiple nuclear and synaptic layers, enabling the maintenance of retinal ganglion and bipolar cells and moreover allowed the development of subtypes as revealed by the single cell RNA-Seq analysis. Ketorolac, Digoxin, Thioridazine, Sildenafil, Ethanol and Methanol were used to screen drug effects on retinal organoids. Exposure of the hPSC-derived retinal organoids to Diogxin, Thioridazine and Sildenafil exposure resulted in photoreceptor cell death, while Digoxin and Thioridazine additionally affected all other cell types, including Müller glia cells. Ethanol and Methanol caused an upregulation in retinal ganglion cell related geneexpression. All drug treatments activated astrocytes, indicated by dendrites sprouting into neuroepithelium and upregulation of astrocyte related genes. The ability to resond to light was presereved in organoids although the number of active retinal ganglion cells decreased after drug expsoure. These data indicate comparable drug effects in organoids to those reported in in vitro models and/or in humans, thus providing first robust experimental evidence of their suitability for toxicological studies.

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Project description:Sequencing of drug resistant organoids

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RNA sequencing of human gastric cancer drug treatment organoids

Project description:Using RNA sequencing, we profile transcriptome dervied from human gastric cancer organoids after drug treatment.

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The RNA-binding protein Hdlbp/Vigilin is increased in hepatic steatosis and regulates VLDL secretion through modulation of Apob mRNA translation

Project description:The liver exerts a wide range of essential functions including the synthesis of plasma proteins and the integration of glucose and lipid homeostasis. While the role of transcriptional networks in the tight regulation of these processes has been extensively studied in healthy and disease states, much less is known about post-transcriptional control of gene expression through RNA-binding proteins (RBP). Here, we report that the highly expressed and conserved RBP Hdlbp/Vigilin is upregulated in patients with non-alcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) and in livers of insulin resistant obese mice. Gain and loss of function studies revealed that Vigilin regulates VLDL secretion through the modulation of ApoB mRNA translation. Photoactivatable ribonucleoside-enhanced crosslinking and immunoprecipitation (PAR-CLIP) analysis in primary hepatocytes demonstrated that Vigilin predominantly binds to CU-rich regions in coding sequences of transcripts of further metabolically relevant secretory proteins such as Apob/apoliproteinB, Ahsg/fetuin-A, Apoc3/apolipoproteinC-III, Fn1/fibronectin, Orm1/orosomucoid and Serpina1/alpha-1-antitrypsin. While mRNA levels of these targets did not change, protein levels were substantially decreased upon knockdown of Vigilin. Hepatic long-term knockdown via GalNAc-conjugated siRNAs ameliorated elevated VLDL/LDL levels and the formation of atherosclerotic plaques in Ldlr–/– mice. These studies uncover a role for Vigilin as a key regulator of hepatic Apob translation and secretion through binding to its mRNA and demonstrate the therapeutic potential of inhibiting Vigilin for cardiovascular diseases.

2017-01-01 | GSE78084 | GEO

RNA-sequencing of ApoB-reactive CD4+ T cells in mice

Project description:We report the transcriptome of atherosclerosis-specific murine CD4+ T cells in atherosclerosis that recognize a peptide from ApoB-100, the core protein of low-density lipoprotein (LDL). Our data reveal a unique transcriptome of ApoB-specific T cells that is similar to T-regulatory T cells and changes during disease progression in a pathogenic T-helper type -1 and -17 like transcriptome.

2020-05-21 | GSE149067 | GEO

siRNAs induced long-term liver ApoB mRNA knockdown significantly lowers serum cholesterol in a mouse model with human-like serum lipids

Project description:Increased serum apoB and associated low density lipoprotein cholesterol (LDL) levels are well correlated with an increased risk of coronary disease. Apo E-/- and LDLr -/- mice have been extensively used for studies of coronary atherosclerosis. These animals show atherosclerotic lesions similar to those in humans, but their serum lipids are low in apoB containing LDL particles. We describe the development of a new mouse model with a human-like lipid profile. Ldlr+/- CETP+/- hemizygous mice carry a single copy of the human CETP transgene and a single copy of a LDL receptor mutation. To evaluate the apoB pathways in this mouse model, we used novel siRNAs formulated in lipid nanoparticles (LNPs). ApoB siRNAs induced up to 95% reduction of liver ApoB mRNA and serum apoB protein, and a significant lowering of serum LDL in Ldlr+/- CETP+/- mice. ApoB targeting is specific, dose dependent and shows lipid lowering effects for over three weeks. Although specific TGs were affected by ApoB KD, and the total plasma lipid levels were decreased by 70%, the overall lipid distribution did not change. Results presented here demonstrate a new mouse model for investigating additional targets within the ApoB pathways using the siRNA modality. Two oligoes specific for ApoB were used to knock down apoB expression in C57Bl6 or B6-Ldlr(tm1)Tg(APOA1-CETP) mice. Gene expression profiling was performed with Affymetrix Merck Custom Mouse 1.0 microarrays (GPL9734).

2010-11-22 | E-GEOD-23088 | biostudies-arrayexpress

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