Reduction of neuronal activity mediated by blood-vessel regression in the adult brain
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1259991 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR33463947.fastq.gz | Fastqsanger.gz | |||
| SRR33463948.fastq.gz | Fastqsanger.gz | |||
| SRR33463949.fastq.gz | Fastqsanger.gz | |||
| SRR33463950.fastq.gz | Fastqsanger.gz | |||
| SRR33463951.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 32 |
Similar Datasets
Project description:To explore the role of brain vascular TAK1 and its functional mechanism , we performed RNA-seq between Cdh5-CreER::Tak1fl/fl mice and their littermate control mice at the age of 12–14 weeks to identify the expression of some unique genes and possible pathway related to the function of brain vascular TAK1. We confirmed the role of brain vascular TAK1 contributed to Glutamate neuronal survival and activity.
2025-05-08 | GSE296574 | GEO
Project description:METTL5 deficiency induces lung cancer regression via mitochondrial translation reduction
| PRJNA1136550 | ENA
Project description:Blood vessel-resident macrophages safeguard blood and vessel integrity in zebrafish
| PRJNA1260425 | ENA
Project description:Macrophages are essential in immune defence, tissue development and maintenance, and are involved in disease onset and progression. Their function is influenced by their microenvironment and origin. While tissue-resident macrophages originate from yolk sac progenitors and persist in some adult tissues through self-renewal, no dedicated macrophage population is known to function within the vast network of blood vessels, despite the importance of maintaining a healthy vascular and blood system. Here, using high spatiotemporal live imaging of zebrafish embryos, we identified a distinctive population of macrophages residing within blood vessels, which we term blood vessel-resident macrophages (bMs). bMs actively survey the bloodstream, clearing foreign particles and unfit cells, and are the first responders to endothelial damage. bMs emerge directly from axial vessels through an atypical endothelial-to-macrophage transition (EMacT), independent of Runx1 and Csf1r, both essential for hematopoiesis and myelopoiesis, respectively. We further demonstrate that bMs are evolutionary conserved in mice. Our data thus unveil the existence of a specialized population of macrophages that function within the vasculature to safeguard blood from foreign threats and maintain blood vessel integrity. These discoveries broaden our understanding of immune surveillance, opening new avenues for treating bloodborne and vascular diseases.
2026-03-10 | GSE296640 | GEO
Project description:The microvasculature plays a key role in tissue perfusion, transport of mediators, and exchange of gases and metabolites to and from tissues. Microvascular dysfunction has emerged as an important contributor to cardiovascular diseases. In this study we used human blood vessel organoids (BVOs) as a model of the microvasculature to delineate the mechanisms of microvascular dysfunction caused by metabolic rewiring. BVOs fully recapitulated key features of the normal human microvasculature, including reliance of mature endothelial cells (ECs) on glycolytic metabolism, as concluded from metabolic flux assays using 13C-glucose labelling and mass spectrometry-based metabolomics. Pharmacological targeting of PFKFB3, a potent activator of glycolysis, with two different chemical inhibitors resulted in rapid BVO restructuring, vessel regression with reduced pericyte coverage. PFKFB3 mutant BVOs also displayed similar structural remodelling compared to control BVOs. Proteomic analysis of the BVO secretome revealed remodelling of the extracellular matrix and differential expression of paracrine mediators such as CTGF. Treatment with recombinant CTGF recovered tight junction formation and increased pericyte coverage in microvessels. Our metabolic and proteomics findings demonstrate that BVOs rapidly undergo restructuring in response to metabolic changes and identify CTGF as a critical paracrine regulator of microvascular integrity.
2023-09-13 | PXD041780 | Pride
Project description:Neutralizing factors involved in blood vessel dysfunction offer a promising strategy for stroke recovery. Many extracellular proteins need enzymatic activation to function, and blocking this activation is an untapped approach to restoring vessel integrity. Here, we demonstrate that inhibition of the extracellular protease SKI-1 with PF-429242 restores blood-vessel integrity and promotes functional recovery in both large- and small-animal models for stroke. Single-cell mRNA sequencing identified molecular signatures suggesting that PF-429242 restores the expression of genes involved in vessel integrity in endothelial cells. Moreover, we identify a mechanism whereby RGMa cleavage by SKI-1 is required for RGMa to interact with Neogenin and alter vessel integrity. Either preventing RGMa cleavage or deleting Neogenin on endothelial cells reduced blood vessel dysfunction, increased tissue preservation, and restored brain function following stroke. This work identifies a much-needed therapeutic strategy which restores blood vessel integrity and functionality, showing efficacy in small- and large-animals.
2025-07-01 | GSE300442 | GEO
Project description:Aberrant lymphatic system function has been increasingly implicated in pathologies such as lymphedema, organ transplant rejection, cardiovascular disease, obesity, and neurodegenerative diseases including Alzheimer's disease and Parkinson's disease. While some pathologies are exacerbated by lymphatic vessel regression and dysfunction, induced lymphatic regression could be therapeutically beneficial in others. Despite its importance, our understanding of lymphatic vessel regression is far behind that of blood vessel regression. Herein, we review the current understanding of blood vessel regression to identify several hallmarks of this phenomenon that can be extended to further our understanding of lymphatic vessel regression. We also summarize current research on lymphatic vessel regression and an array of research tools and models that can be utilized to advance this field. Additionally, we discuss the roles of lymphatic vessel regression and dysfunction in select pathologies, highlighting how an improved understanding of lymphatic vessel regression may yield therapeutic insights for these disease states.
| S-EPMC8980686 | biostudies-literature
Project description:Serum-free samples are prepared from explant culture of bovine periosteum and compared with blood vessel specific proteins.
2024-09-20 | PXD053777 | JPOST Repository
Project description:Serum-free samples are prepared from explant culture of bovine periosteum and compared with blood vessel specific proteins.
2024-09-20 | PXD054612 | JPOST Repository
Project description:Macrophages are essential in immune defence, tissue development, and disease onset and progression. Their function is in part dictated by their microenvironment and origin. Tissue-resident macrophages originate from yolk sac progenitors, persisting in adult organs and tissues mainly through self-renewal. Although ubiquitously present throughout the body, no dedicated macrophage population is known to function within the vast network of blood vessels, despite the importance of maintaining a healthy vascular and blood system. Here, we identified a distinctive population of macrophages residing within blood vessels, which we termed blood-resident macrophages (bMΦ). bMΦ actively survey the blood to eliminate foreign particles and unfit cells, and act as the first responders to endothelial damage. bMΦ emerge directly from the main axial vessels of zebrafish embryos though an atypical endothelial-to-macrophage transition (EMacT), independent of Runx1 and Csf1r, both essential for hematopoietic stem cell and myeloid cell production, respectively. Our data thus unveil the existence of a specialized population of macrophages that function within the confinement of the vasculature to safeguard blood from foreign threats and maintain blood vessel integrity. These discoveries not only expand our understanding of immune surveillance mechanisms but also offer potential avenues for the treatment of bloodborne diseases and vascular injuries.
2026-03-11 | PXD052344 | Pride