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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE149067 | GEO | 2020/05/21

REPOSITORIES: GEO

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Single cell sequencing of murine ApoB-reactive CD4+ T cells

Project description:We report the single cell transcriptome of atherosclerosis-specific murine CD4+ T cells that recognize a peptide from ApoB-100, the core protein of low-density lipoprotein (LDL). Our data reveal a unique single cell transcriptome of ApoB-specific T cells that is similar to T-regulatory T but shows an overlap with the transcriptome of pathogenic T-helper type -1 and -17 cells on a single cell level.

2020-05-21 | GSE149068 | 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

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

2010-11-22 | GSE23088 | 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.

2022-05-24 | GSE174227 | GEO

Pathogenic autoimmunity in atherosclerosis evolves from initially protective ApoB-reactive CD4+ T-regulatory cells

Project description:Pathogenic autoimmunity in atherosclerosis evolves from initially protective ApoB-reactive CD4+ T-regulatory cells

| PRJNA627234 | ENA

Kupffer cells dictate hepatic responses to the atherogenic dyslipidemic insult

Project description:Apolipoprotein-B (APOB)-containing lipoproteins cause atherosclerosis. Whether the vasculature is initially responding site, or if atherogenic-dyslipidemia affects other organs simultaneously, is unknown. Here we show that the liver responds to a dyslipidemic insult based on inducible models of familial hypercholesterolemia and APOB tracing. An acute transition to atherogenic APOB-lipoprotein levels resulted in uptake by Kupffer cells and rapid accumulation of triglycerides and cholesterol in the liver. Bulk and single-cell RNA-seq revealed an Kupffer cell-specific transcriptional program that was not activated by a high-fat diet alone, or detected in standard liver function or pathological assays, even in the presence of fulminant atherosclerosis. Depletion of Kupffer cells altered the dynamic of plasma and liver lipid concentrations, indicating that these liver macrophages help restrain and buffer atherogenic lipoproteins, whilst simultaneously secreting atherosclerosis-modulating factors into plasma. Our results place Kupffer cells as key sentinels in organizing systemic responses to lipoproteins at the initiation of atherosclerosis.

2024-02-05 | GSE254879 | GEO

Kupffer cells dictate hepatic responses to the atherogenic dyslipidemic insult (scRNA-Seq)

2024-02-05 | GSE254971 | GEO

CD4 T cell response to MHC-II-restricted APOB epitope in human cardiovascular disease revealed by single cell transcriptomics and TCR reconstruction

Project description:We sorted T-helper-1 (Th1), memory (Tmem), Treg and APOB-specific CD4 T cells, detected and sorted by a validated MHC-II tetramer DRB1*07:01 APOB-p18 (Tet+ cells) from peripheral blood mononuclear cell samples from 8 DRB1*07:01+ women with and without subclinical cardiovascular disease (sCVD) as documented by carotid artery ultrasound. We subjected them to 10x Genomics 5’ single cell RNA-sequencing with T cell receptor (TCR) sequencing.

2022-03-26 | GSE199103 | GEO

Atlas of miRNome variations in different dyslipidemic conditions: a study in C57Bl/6, Ldlr-KO, and Pcsk9-KO mice.

Project description:In this study, mice with different genotypes and fed diets with different lipid content were enrolled, aiming to set up an atlas of miRNA expression levels in different organs with a relevant role in lipid/lipoprotein metabolism. Specifically, three genotypes were investigated: C57Bl/6 mice as controls, together with mice knock-out (KO) for LDLr (low-density lipoprotein receptor) and for PCSK9 (proprotein convertase subtilisin/kexin type 9). LDLr and PCSK9 are both involved in LDL turnover, the former mediating LDL clearance [PMID: 19299327], the latter causing the degradation of the LDLr protein [PMID: 17080197]. As a result, LDLrKO mice, because of their impaired LDL catabolism, are hypercholesterolemic and prone to atherosclerosis development, particularly when fed high-fat, cholesterol-containing diets [PMID: 8349823; PMID: 8182121]. On the contrary, PCSK9KO mice, characterized by an accelerated LDL catabolism, are hypocholesterolemic and atherosclerosis resistant [PMID: 15805190]. miRNA expression was investigated in liver, intestine, aorta, white adipose tissue and brain of mice on both standard and Western diet.

2023-09-06 | GSE227578 | GEO

Qualitative analysis of oxidative modifications of apolipoprotein amino acid residues in in vivo-oxidized lipoprotein that is increased in patients with acute myocardial infarction

Project description:Oxidized low-density lipoprotein (oxLDL) is a known risk factor for atherogenesis. However, it is not clear what are the key components of oxLDL driving atherosclerosis.This study aimed to reveal structural features of oxLDL present in circulation of patients with acute myocardial infarction (AMI) and healthy subjects. Total LDL and HDL were separated from pooled sera prepared from 3-6 indivisuals of 25 AMI patients and plasma of seven healthy subjects using ultracentrifugation.When LDL was fractionated on an anion-exchange column, in vivo-oxLDL of AMI patients and healthy subjects, detected by the anti-oxidized phosphatidylcholine (oxPC) monoclonal antibody, was concentrated in electronegative LDL (LDL(-)) fraction. Surprisingly, LDL(-) fraction contained HDL-sized particles in addition to LDL observed using transmission electron microscopy. LC-MS/MS revealed this fraction contaned oxidized apolipoprotein A1 (apoA1) and all lysine residues of the oxidized apoA1 were modified by acrolein. The electronegative in vivo-oxLDL was immunologically purified from the LDL(-) fraction with an anti-oxPC monoclonal antibody, and LC-MS/MS analysis carried out to explore oxidatively modified peptides; but only a small number of acrolein-modified residues identified in the apoB. We propose that oxidized HDL interacts with in vivo-oxLDL that is involved in atherosclerosis.

2020-03-10 | PXD017957 | JPOST Repository

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