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Paternal hypercholesterolemia elicits sex-specific exacerbation of atherosclerosis in adult offspring of LDL receptor-deficient mice

ABSTRACT: Paternal hypercholesterolemia elicits sex-specific exacerbation of atherosclerosis in adult offspring of LDL receptor-deficient mice

PROVIDER: PRJNA1055098 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27308004_1.fastq.gz	Fastqsanger.gz
	SRR27308004_2.fastq.gz	Fastqsanger.gz
	SRR27308005_1.fastq.gz	Fastqsanger.gz
	SRR27308005_2.fastq.gz	Fastqsanger.gz
	SRR27308006_1.fastq.gz	Fastqsanger.gz

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Paternal hypercholesterolemia elicits sex-specific exacerbation of atherosclerosis in adult offspring of LDL receptor-deficient mice

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Impaired adult hippocampal neurogenesis in a mouse model of familial hypercholesterolemia: a role for the LDL receptor and cholesterol metabolism in adult neural precursor cells (LDL treatment)

Project description:In familial hypercholesterolemia (FH), mutations in the low-density lipoprotein (LDL) receptor (LDLr) gene result in increased plasma LDL cholesterol. Clinical and preclinical studies revealed an association between FH and hippocampus-related memory and mood impairment. We here asked whether hippocampal pathology in FH might be a consequence of compromised adult hippocampal neurogenesis. We evaluated hippocampus-dependent behaviour and neurogenesis in adult C57BL/6JRj and LDLr-/- mice. Behavioural tests revealed that adult LDLr-/- mice showed reduced performance in a dentate gyrus (DG)-dependent metric change task. This phenotype was accompanied by a reduction in cell proliferation and adult neurogenesis in the DG of LDLr-/- mice, suggesting a potential direct impact of LDLr mutation on NPC. We thus investigated the effects of elevated cholesterol and the function of LDLr in neural precursor cells (NPC) isolated from adult C57BL/6JRj mice in vitro. Exposure of NPC to LDL as well as LDLr gene knockdown reduced proliferation and disrupted transcriptional activity of genes involved in endogenous cholesterol synthesis and metabolism. The LDL treatment also induced an increase in intracellular lipid storage. Functional analysis of differentially expressed genes revealed parallel modulation of distinct regulatory networks upon LDL treatment and LDLr knockdown. Together, these results suggest that high LDL levels and a loss of LDLr function, which are characteristic to individuals with FH, might contribute to a disease-related impairment in adult hippocampal neurogenesis and, consequently, cognitive functions.

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Transcription profiling of macrophages from Familial Hypercholesterolemia(FH) patients with tendon xanthomas (TX+) and without tendon xanthomas (TX-) to evaluate the gene expression profile in presence and absence of oxidized LDL

Project description:Total RNA pools from macrophages from Familial Hypercholesterolemia(FH) patients with tendon xanthomas (TX+) and without tendon xanthomas (TX-) were analyzed using Affymetrix oligonucleotide arrays (HGU133A) to evaluate the gene expression profile in presence and absence of oxidized LDL.

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Impact of inducing hypercholesterolemia on Kupffer cells

Project description:Kupffer cells (KCs) are the largest tissue resident macrophage population in direct contact with blood and thus with circulating lipoproteins. How KCs homeostasis is affected by the build-up of cholesterol-rich lipoproteins in the context of hypercholesterolemia has been poorly investigated. In this study, 5-month-old LDL receptor deficient (C57BL6J background) male mice were subjected to chow diet or a cholesterol-rich (HC) diet for four days to induce hypercholesterolemia. RNA sequencing was then performed on cell sorted KCs.

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Impaired adult hippocampal neurogenesis in a mouse model of familial hypercholesterolemia: a role for the LDL receptor and cholesterol metabolism in adult neural precursor cells (LDLR Knockdown)

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Imprints of atherosclerosis are present in circulating T cells of patients with Familial Hypercholesterolemia

Project description:Atherosclerosis is the major cause of death in industrialized countries. This disease has initially been characterized as a lipid disorder, but current concepts argue for an inflammatory disease, which develops in the background of hypercholesterolemia and other risk factors. In response to initial events of atherosclerosis formation, such as LDL-deposition in the subendothelial space, monocytes and T cells interact with the vessel wall. However, little is known about the properties and the behavior of these cells in this context. Using familial hypercholesterolemia (FH) as a model we demonstrate substantial differences in the gene expression of freshly isolated human monocytes and T lymphocytes. In FH monocytes we found an increased uptake of oxidized LDL, elevated amounts of scavenger receptors and adhesion molecules, and differences in the regulation of intracellular lipoprotein metabolism compared to monocytes from healthy individuals. Furthermore, the monocyte subpopulation of CD14+/CD16+ cells is less frequent in FH but exhibits significantly higher levels of CD11c and CD29 which increases the likelihood for their transmigration through the endothelial layer. The presence of increased amounts of CD69 in T lymphocytes from FH patients suggests that these cells are more activated than control cells. Our results indicate that some important steps of atherosclerosis formation already take place in circulating blood cells which extends current atherosclerosis models to the plasma compartment. Keywords: atherosclerosis, T cells, Familial Hypercholesterolemia

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Transcription profiling of human circulating monocytes from patients with familial hypercholesterolemia

Project description:Atherosclerosis is the major cause of death in industrialized countries. This disease has initially been characterized as a lipid disorder, but current concepts argue for an inflammatory disease, which develops in the background of hypercholesterolemia and other risk factors. In response to initial events of atherosclerosis formation, such as LDL-deposition in the subendothelial space, monocytes and T cells interact with the vessel wall. However, little is known about the properties and the behavior of these cells in this context. Using familial hypercholesterolemia (FH) as a model we demonstrate substantial differences in the gene expression of freshly isolated human monocytes and T lymphocytes. In FH monocytes we found an increased uptake of oxidized LDL, elevated amounts of scavenger receptors and adhesion molecules, and differences in the regulation of intracellular lipoprotein metabolism compared to monocytes from healthy individuals. Furthermore, the monocyte subpopulation of CD14+/CD16+ cells is less frequent in FH but exhibits significantly higher levels of CD11c and CD29 which increases the likelihood for their transmigration through the endothelial layer. The presence of increased amounts of CD69 in T lymphocytes from FH patients suggests that these cells are more activated than control cells. Our results indicate that some important steps of atherosclerosis formation already take place in circulating blood cells which extends current atherosclerosis models to the plasma compartment. Experiment Overall Design: 25 monocytes samples: 5 homozygous FH, 7 heterozygous FH, 13 control participants

2008-06-14 | E-GEOD-6054 | biostudies-arrayexpress

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Expression data from ARPE-19 cells treated with LDL or ox-LDL

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2006-09-01 | E-GEOD-5741 | biostudies-arrayexpress

Impaired adult hippocampal neurogenesis in a mouse model of familial hypercholesterolemia: a role for the LDL receptor and cholesterol metabolism in adult neural precursor cells (LDL treatment)

Project description:Impaired adult hippocampal neurogenesis in a mouse model of familial hypercholesterolemia: a role for the LDL receptor and cholesterol metabolism in adult neural precursor cells (LDL treatment)

| PRJNA563678 | ENA

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