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Microglia regulate basal cerebral blood flow and neurovascular coupling through ectonucleotidase CD39

ABSTRACT: Microglia regulate basal cerebral blood flow and neurovascular coupling through ectonucleotidase CD39

PROVIDER: PRJNA925565 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23137712_1.fastq.gz	Fastqsanger.gz
	SRR23137712_2.fastq.gz	Fastqsanger.gz
	SRR23137713_1.fastq.gz	Fastqsanger.gz
	SRR23137713_2.fastq.gz	Fastqsanger.gz
	SRR23137714_1.fastq.gz	Fastqsanger.gz

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Microglia regulate basal cerebral blood flow and neurovascular coupling through ectonucleotidase CD39

Project description:Microglia tightly interact with brain capillaries and regulate blood brain barrel permeability in pathological conditions. However, it is still unknown whether and how microglia regulate CBF in homeostatic condition. Here we show microglia directly regulate cerebral blood flow (CBF) and neurovascular coupling. Conditional knockout of microglial CD39 resulted in CBF hyper perfusion, reduced ATP induced CBF increase, impaired neurovascular coupling by whisker stimulation and reduced whisker stimulation induced adenosine increase in barrel cortex. Out data suggest that microglia is an important player for CBF regulation.

2023-07-01 | GSE223314 | GEO

Microglia modulate the cerebrovascular reactivity through ectonucleotidase CD39

Project description:Microglia and the border-associated macrophages contribute to the modulation of cerebral blood flow, but the mechanisms have remained uncertain. Here, we show that microglia regulate the cerebral blood flow baseline and the responses to whisker stimulation or intra-cisternal magna injection of adenosine triphosphate, but not intra-cisternal magna injection of adenosine in mice model. Notably, microglia repopulation corrects these cerebral blood flow anomalies. The microglial-dependent regulation of cerebral blood flow requires the adenosine triphosphate-sensing P2RY12 receptor and ectonucleotidase CD39 that initiates the dephosphorylation of extracellular adenosine triphosphate into adenosine in both male and female mice. Pharmacological inhibition or CX3CR1-CreER-mediated deletion of CD39 mimics the cerebral blood flow anomalies in microglia-deficient mice and reduces the upsurges of extracellular adenosine following whisker stimulation. Together, these results suggest that the microglial CD39-initiated breakdown of extracellular adenosine triphosphate co-transmitter is an important step in neurovascular coupling and the regulation of cerebrovascular reactivity.

2024-06-01 | GSE245107 | GEO

Microglia modulate the cerebrovascular reactivity through ectonucleotidase CD39

Project description:Microglia modulate the cerebrovascular reactivity through ectonucleotidase CD39

| PRJNA1026953 | ENA

Endothelial-neuronal coupling revealed in a decoupled neurovascular unit based Organ-on-Chip approach.

Project description:This data set is for the article: Endothelial-neuronal coupling revealed in a decoupled neurovascular unit based Organ-on-Chip approach.

2017-08-24 | MSV000081480 | MassIVE

Synaptic-like transmission between neural axons and arterial smooth muscle cells drives cerebral neurovascular coupling

Project description:Normally functioning brains depend on neurovascular coupling (NVC) and its dysfunction underlies many neuropathologies. Although cell-type specificity has been implicated in NVC, how active neural information is specifically conveyed to the targeted arterioles in the brain remains poorly understood. Here, using two-photon focal optogenetics in the mouse cerebral cortex, we demonstrated that single glutamatergic axons dilate their innervating arterioles via synaptic-like transmission between neural-arteriolar smooth muscle cells junction (NsMJ). The presynaptic parental-daughter bouton makes dual innervations on postsynaptic dendrites and on arteriolar smooth muscles cells (aSMCs), which expressed many types of neuromediator receptors, including glutamate NMDA receptor subunit 1 (Grin1). Disruption of NsMJ transmission, by aSMC specific knockout of GluN1, diminished the optogenetic and whisker stimulation-caused functional hyperemia. Notably, the absence of GluN1 subunit in aSMCs protected the brain atrophy from cerebral ischemia by preventing Ca2+ overload in aSMCs during arteriolar constriction caused by the ischemia-induced spreading depolarization. Our findings reveal that NsMJ transmission drives neurovascular coupling and also open up a new avenue for studying stroke.

2023-10-05 | GSE213026 | GEO

RNA-Seq of FACS-sorted, KIR-CD39-,KIR+CD39- and KIR+CD39+, Uterine NK cells (uNK cells) from human decidual samples

Project description:Uterine NK cells (uNK cells) form a distinct immune cell population in the endometrium and decidua. Here, we FACS-sorted KIR-CD39-,KIR+CD39- and KIR+CD39+ uNK cells from decidual samples.

2021-02-19 | E-MTAB-8709 | biostudies-arrayexpress

Ectonucleotidase CD39 is highly expressed on ATLL cells and is responsible for their immunosuppressive function.

Project description:Ectonucleotidase CD39 is highly expressed on ATLL cells and is responsible for their immunosuppressive function.

| PRJNA524298 | ENA

PLA2G4A promotes right-sided colorectal cancer progression by inducing CD39+γδ Tregs polarization

Project description:Here, we discovered that the frequency of CD39+γδ Tregs, which positively correlated with poor prognosis, was significantly higher in right-sided colorectal cancer (RSCRC) than in the left-sided CRC (LSCRC). To explore the molecular mechanism leading to the difference of CD39+γδ Tregs derived from RSCRC and LSCRC, we collected fresh tissue samples of RSCRC with high expression of CD39+γδ Tregs and the LSCRC with low expression of CD39+γδ Tregs detected by flow cytometry and identified differential proteins by LC-MS based quantitative proteomic analysis with tandem mass tag (TMT)

2022-02-17 | PXD027323 | Pride

NTPDase1/CD39 Ectonucleotidase Is Necessary for Normal Arterial Diameter Adaptation to Flow.

Project description:NTPDase1/CD39, the major vascular ectonucleotidase, exerts thrombo-immunoregulatory function by controlling endothelial P2 receptor activation. Despite the well-described release of ATP from endothelial cells, few data are available regarding the potential role of CD39 as a regulator of arterial diameter. We thus investigated the contribution of CD39 in short-term diameter adaptation and long-term arterial remodeling in response to flow using Entpd1-/- male mice. Compared to wild-type littermates, endothelial-dependent relaxation was modified in Entpd1-/- mice. Specifically, the vasorelaxation in response to ATP was potentiated in both conductance (aorta) and small resistance (mesenteric and coronary) arteries. By contrast, the relaxing responses to acetylcholine were supra-normalized in thoracic aortas while decreased in resistance arteries from Entpd1-/- mice. Acute flow-mediated dilation, measured via pressure myography, was dramatically diminished and outward remodeling induced by in vivo chronic increased shear stress was altered in the mesenteric resistance arteries isolated from Entpd1-/- mice compared to wild-types. Finally, changes in vascular reactivity in Entpd1-/- mice were also evidenced by a decrease in the coronary output measured in isolated perfused hearts compared to the wild-type mice. Our results highlight a key regulatory role for purinergic signaling and CD39 in endothelium-dependent short- and long-term arterial diameter adaptation to increased flow.

| S-EPMC10606763 | biostudies-literature

Tuning the Thromboinflammatory Response to Venous Flow Interruption by the Ectonucleotidase CD39.

Project description:Objective- Leukocyte flux contributes to thrombus formation in deep veins under pathological conditions, but mechanisms that inhibit venous thrombosis are incompletely understood. Ectonucleotide di(tri)phosphohydrolase 1 ( ENTPD1 or Cd39), an ectoenzyme that catabolizes extracellular adenine nucleotides, is embedded on the surface of endothelial cells and leukocytes. We hypothesized that under venous stasis conditions, CD39 regulates inflammation at the vein:blood interface in a murine model of deep vein thrombosis. Approach and Results- CD39-null mice developed significantly larger venous thrombi under venous stasis, with more leukocyte recruitment compared with wild-type mice. Gene expression profiling of wild-type and Cd39-null mice revealed 76 differentially expressed inflammatory genes that were significantly upregulated in Cd39-deleted mice after venous thrombosis, and validation experiments confirmed high expression of several key inflammatory mediators. P-selectin, known to have proximal involvement in venous inflammatory and thrombotic events, was upregulated in Cd39-null mice. Inferior vena caval ligation resulted in thrombosis and a corresponding increase in both P-selectin and VWF (von Willebrand Factor) levels which were strikingly higher in mice lacking the Cd39 gene. These mice also manifest an increase in circulating platelet-leukocyte heteroaggregates suggesting heterotypic crosstalk between coagulation and inflammatory systems, which is amplified in the absence of CD39. Conclusions- These data suggest that CD39 mitigates the venous thromboinflammatory response to flow interruption.

| S-EPMC6467508 | biostudies-literature

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