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Microglia are not necessary for maintenance of blood-brain barrier properties in health, but PLX5622 alters brain endothelial cholesterol metabolism (Astro Seq)

ABSTRACT: Microglia are not necessary for maintenance of blood-brain barrier properties in health, but PLX5622 alters brain endothelial cholesterol metabolism (Astro Seq)

PROVIDER: PRJNA1111904 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29044918_1.fastq.gz	Fastqsanger.gz
	SRR29044918_2.fastq.gz	Fastqsanger.gz
	SRR29044919_1.fastq.gz	Fastqsanger.gz
	SRR29044919_2.fastq.gz	Fastqsanger.gz
	SRR29044920_1.fastq.gz	Fastqsanger.gz

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Microglia are not necessary for maintenance of blood-brain barrier properties in health, but PLX5622 alters brain endothelial cholesterol metabolism (Liver Seq)

Project description:Microglia are resident immune cells of the central nervous system, yet their functions far exceed those related to immunology. From pruning neural synapses during development to preventing excessive neural activity throughout life, microglia are intimately involved in the brain’s most basic processes. Studies have reported a close interaction between microglia and endothelial cells, as well as both helpful and harmful roles for microglia at the blood-brain barrier (BBB) in the context of disease. However, much less work has been done to understand microglia-endothelial cell interactions in the healthy brain. Here, we aim to determine the role of microglia at the healthy BBB. We used the colony-stimulating factor 1 receptor (CSF1R) inhibitor PLX5622 to deplete microglia and analyzed BBB ultrastructure, permeability, and transcriptome. Interestingly, we found that, despite their direct contact with endothelial cells, microglia are not necessary for maintenance of BBB structure, function, or gene expression in the healthy brain. However, we found that PLX5622 treatment alters brain endothelial cholesterol metabolism, and this effect was independent from microglial depletion, suggesting PLX5622 has off-target effects on brain vasculature.

2024-05-22 | GSE267594 | GEO

Microglia are not necessary for maintenance of blood-brain barrier properties in health, but PLX5622 alters brain endothelial cholesterol metabolism (Astro Seq)

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Microglia are not necessary for maintenance of blood-brain barrier properties in health, but PLX5622 alters brain endothelial cholesterol metabolism (Brain Endo SC Seq)

2024-05-22 | GSE267591 | GEO

Microglia are not necessary for maintenance of blood-brain barrier properties in health, but PLX5622 alters brain endothelial cholesterol metabolism (Brain Endo Bulk Seq)

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Microglia are not necessary for maintenance of blood-brain barrier properties in health, but PLX5622 alters brain endothelial cholesterol metabolism (Liver Seq)

Project description:Microglia are not necessary for maintenance of blood-brain barrier properties in health, but PLX5622 alters brain endothelial cholesterol metabolism (Liver Seq)

| PRJNA1111909 | ENA

Microglia are not necessary for maintenance of blood-brain barrier properties in health, but PLX5622 alters brain endothelial cholesterol metabolism (Brain Endo Bulk Seq)

Project description:Microglia are not necessary for maintenance of blood-brain barrier properties in health, but PLX5622 alters brain endothelial cholesterol metabolism (Brain Endo Bulk Seq)

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Microglia are not necessary for maintenance of blood-brain barrier properties in health, but PLX5622 alters brain endothelial cholesterol metabolism (Brain Endo SC Seq)

Project description:Microglia are not necessary for maintenance of blood-brain barrier properties in health, but PLX5622 alters brain endothelial cholesterol metabolism (Brain Endo SC Seq)

| PRJNA1111903 | ENA

Diabetes and Insulin in Regulation of Brain Cholesterol Metabolism

Project description:The brain is the most cholesterol-rich organ in the body, most of which comes from in situ synthesis. Here we demonstrate that in insulin-deficient diabetic mice, there is a reduction in expression of the major transcriptional regulator of cholesterol metabolism, SREBP-2, and its downstream genes in the hypothalamus and other areas of the brain, leading to a reduction in brain cholesterol synthesis and synaptosomal cholesterol content. These changes are due, at least in part, to direct effects of insulin to regulate these genes in neurons and glial cells and can be corrected by intracerebroventricular injections of insulin. Knockdown of SREBP-2 in cultured neurons causes a decrease in markers of synapse formation and reduction of SREBP-2 in the hypothalamus of mice using shRNA results in increased feeding and weight gain. Thus, insulin and diabetes can alter brain cholesterol metabolism, and this may play an important role in the neurologic and metabolic dysfunction observed in diabetes and other disease states. Hypothalamus was compared between streptozotocin (STZ)-induced diabetic, ob/ob, and control mice, with 5-6 replicates per goup.

2014-10-03 | E-GEOD-62013 | biostudies-arrayexpress

ORP6 regulates astrocytic cholesterol metabolism and brain Aβ deposition

Project description:The mammalian brain is the most cholesterol-rich organ of the body, requiring in situ de novo cholesterol synthesis to meet this demand. Defects in brain cholesterol homeostasis are implicated in cognitive deficits related to aging and in neurodegenerative diseases, such as Alzheimer’s Disease (AD). Oxysterol-binding protein (OSBP)-related proteins (ORPs) are highly conserved cytosolic proteins that coordinate lipid homeostasis by regulating cell signaling, inter-organelle membrane contact sites and non-vesicular transport of cholesterol. Here, we show that ORP6 is highly expressed in the brain, where it exhibits spatial and cell-type specific expression. ORP6 expression is enriched in the hippocampus and caudal-putamen brain regions, specifically within neurons and astrocytes. ORP6 knockdown in astrocytes altered the expression of cholesterol biosynthesis, cholesterol efflux and cholesterol esterification genes, resulting in the accumulation of esterified cholesterol within cellular lipid droplets and reduced cholesterol efflux. Furthermore, ORP6 ablation in mice resulted in dysregulation of whole body lipid homeostasis, increased brain desmosterol and Aβ deposition, and cognitive impairment. Our findings highlight a critical role for ORP6 in brain cholesterol homeostasis and identify ORP6 as a potential novel target for the treatment of AD.

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Diabetes and Insulin in Regulation of Brain Cholesterol Metabolism

2014-10-03 | GSE62013 | GEO