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Aged blood impairs hippocampal neural precursor activity and activates microglia via brain endothelial cell VCAM1

ABSTRACT: Aged blood impairs hippocampal neural precursor activity and activates microglia via brain endothelial cell VCAM1

PROVIDER: PRJNA525880 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8691140_1.fastq.gz	Fastqsanger.gz
	SRR8691140_2.fastq.gz	Fastqsanger.gz
	SRR8691150_1.fastq.gz	Fastqsanger.gz
	SRR8691150_2.fastq.gz	Fastqsanger.gz
	SRR8691160_1.fastq.gz	Fastqsanger.gz

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Aged blood impairs hippocampal neural precursor activity and activates microglia via brain endothelial cell VCAM1

Project description:Aged blood impairs hippocampal neural precursor activity and activates microglia via brain endothelial cell VCAM1

| PRJNA525299 | ENA

Aged blood impairs hippocampal neural precursor activity and activates microglia via brain endothelial cell VCAM1.

Project description:An aged circulatory environment can activate microglia, reduce neural precursor cell activity and impair cognition in mice. We hypothesized that brain endothelial cells (BECs) mediate at least some of these effects. We observe that BECs in the aged mouse hippocampus express an inflammatory transcriptional profile with focal upregulation of vascular cell adhesion molecule 1 (VCAM1), a protein that facilitates vascular-immune cell interactions. Concomitantly, levels of the shed, soluble form of VCAM1 are prominently increased in the plasma of aged humans and mice, and their plasma is sufficient to increase VCAM1 expression in cultured BECs and the hippocampi of young mice. Systemic administration of anti-VCAM1 antibody or genetic ablation of Vcam1 in BECs counteracts the detrimental effects of plasma from aged individuals on young brains and reverses aging aspects, including microglial reactivity and cognitive deficits, in the brains of aged mice. Together, these findings establish brain endothelial VCAM1 at the blood-brain barrier as a possible target to treat age-related neurodegeneration.

| S-EPMC6642642 | biostudies-literature

Aged blood impairs hippocampal neural precursor activity and activates microglia via brain endothelial cell VCAM1

Project description:Single cell RNAseq of Old (19 month) and Young (3 month) mouse brain endothelial cells isolated from hippocampi of C57BL6 males.

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Aged blood impairs hippocampal neural precursor activity and activates microglia via brain endothelial cell VCAM1

Project description:RNAseq of Old (19 month) vs Yound (3 month) mouse brain endothelial cells

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Transcriptome outcome of oligodendrocyte precursor cells following VCAM1 knockdown

Project description:Transcriptome outcome of rat oligodendrocyte precursor cells, which were knocked down with short-hairpin RNA (shRNA) for vascular cell adhesion molecule 1 (VCAM1)

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RNA-seq of VCAM1-positive cardiac fibroblasts (VCF) and VCAM1-negative cardiac fibroblasts (VNCF).

Project description:This experiment aims at comparing the transcriptomic profiles of two subpopulations of fetal human cardiac fibroblasts (HCF) defined by their relative expression of VCAM1. VCAM1-positive and VCAM1-negative populations were isolated from commercial fetal HCF by MACS against VCAM1. The RNA-seq procedure was outsourced to GENEWIZ (South Plainfield, NJ, USA), and subsequent analysis was performed in-house. Briefly, total mRNA was captured using the NEBNext Poly(A) mRNA Magnetic Isolation Module, and the library was constructed with the NEBNext Ultra RNA Library Prep Kit for Illumina. Sequencing was realized on an Illumina HiSeq 2500 System.

2020-08-08 | E-MTAB-9161 | biostudies-arrayexpress

The VCAM1–ApoE pathway directs microglial chemotaxis and alleviates Alzheimer’s disease pathology

Project description:In Alzheimer’s disease (AD), sensome receptor dysfunction impairs microglial danger-associated molecular pattern (DAMP) clearance and exacerbates disease pathology. While extrinsic signals including interleukin-33 (IL-33) can restore microglial DAMP clearance, it remains largely unclear how the sensome receptor(s) is regulated and interacts with DAMP during phagocytic clearance. Here, we show that IL-33 induces VCAM1 in microglia, which promotes microglial chemotaxis toward amyloid-beta (Aβ) plaque-associated ApoE, and leads to Aβ clearance. We show that IL-33 stimulates a chemotactic state in microglia, characterized by Aβ-directed migration. Functional screening identified that VCAM1 directs microglial Aβ chemotaxis by sensing Aβ plaque-associated ApoE. Moreover, we found that disrupting VCAM1–ApoE interaction abolishes microglial Aβ chemotaxis, resulting in decreased microglial clearance of Aβ. In patients with AD, higher cerebrospinal fluid levels of soluble VCAM1 were correlated with impaired microglial Aβ chemotaxis. Together, our findings demonstrate that promoting VCAM1–ApoE-dependent microglial functions ameliorates AD pathology.

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Wybutosine hypomodification of tRNAphe activates HERVK and impairs neuronal differentiation

Project description:Wybutosine hypomodification of tRNAphe activates HERVK and impairs neuronal differentiation

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RNA-seq of VCAM1-positive cardiac fibroblasts (VCF) and VCAM1-negative cardiac fibroblasts (VNCF).

Project description:RNA-seq of VCAM1-positive cardiac fibroblasts (VCF) and VCAM1-negative cardiac fibroblasts (VNCF).

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Project description:Endothelial cells (ECs) act as an internal barrier to the vessel wall, hindering the development of inflammation, and only when activated will promote the development of vascular inflammation. However, the heterogeneity of the aortic ECs in the setting of vascular inflammation have not been fully assessed. Here, we defined 4 EC subpopulations, including Cd36+ EC, Notch3+ EC, Vcam1+ EC and Lyve1+ EC. Based on the enrichment analysis, Vcam1+ EC were considered to be a subpopulation of ECs susceptible to activation. After high-fat diet (HFD) intake, decreased expression of Krüppel-like factor 2 (Klf2) occurred only in Vcam1+ EC. Moreover, S1pr1 was validated as a downstream target protein of klf2. Upregulation of Klf2 expression ameliorated vascular ECs inflammation under HFD condition. Our study elucidates the Klf2 in Vcam1+ EC is a critical regulator of vascular inflammation and increases understanding of development and progression of aortic inflammatory disease.

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