Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Functional hypoxia drives neuroplasticity and neurogenesis via brain erythropoietin

ABSTRACT: Functional hypoxia drives neuroplasticity and neurogenesis via brain erythropoietin

PROVIDER: PRJNA603663 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10983721_1.fastq.gz	Fastqsanger.gz
	SRR10983721_2.fastq.gz	Fastqsanger.gz
	SRR10983722_1.fastq.gz	Fastqsanger.gz
	SRR10983722_2.fastq.gz	Fastqsanger.gz
	SRR10983723_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Functional hypoxia drives neuroplasticity and neurogenesis via brain erythropoietin

Project description:Erythropoietin (EPO), named after its role in hematopoiesis, is also expressed in the mammalian brain. In clinical settings, recombinant EPO had revealed a remarkable improvement of cognitive functions, but the underlying mechanisms have remained obscure. Animal studies demonstrated, however, that neuronal EPO effects are independent of an elevated hematocrit. Here, we show with a novel line of reporter mice that cognitive challenge leads to local/endogenous hypoxia in hippocampal pyramidal neurons where it induces enhanced expression of both EPO and EPO receptor (EPOR). High-dose EPO administration, which amplifies auto/paracrine EPO/EPOR signaling, prompts the emergence of new CA1 neurons and enhanced dendritic spine densities. Single cell sequencing reveals rapid increase in newly differentiating neurons. Importantly, improved performance on complex running wheels after EPO treatment is imitated by exposure to mild exogenous/inspiratory hypoxia. All these effects depend on neuronal expression of the Epor gene. Taken together, this suggests a novel cellular model of neuroplasticity in which neuronal networks, challenged by cognitive tasks, drift into transient hypoxia which becomes a trigger of neuronal EPO/EPOR expression. This regulatory circle causes long-lasting neuroplastic adaptation, and as fundamental cellular mechanism, may be relevant for strategies aiming at cognitive improvement.

2020-01-30 | GSE144444 | GEO

Functional hypoxia drives neuroplasticity and neurogenesis via brain erythropoietin.

Project description:Erythropoietin (EPO), named after its role in hematopoiesis, is also expressed in mammalian brain. In clinical settings, recombinant EPO treatment has revealed a remarkable improvement of cognition, but underlying mechanisms have remained obscure. Here, we show with a novel line of reporter mice that cognitive challenge induces local/endogenous hypoxia in hippocampal pyramidal neurons, hence enhancing expression of EPO and EPO receptor (EPOR). High-dose EPO administration, amplifying auto/paracrine EPO/EPOR signaling, prompts the emergence of new CA1 neurons and enhanced dendritic spine densities. Single-cell sequencing reveals rapid increase in newly differentiating neurons. Importantly, improved performance on complex running wheels after EPO is imitated by exposure to mild exogenous/inspiratory hypoxia. All these effects depend on neuronal expression of the Epor gene. This suggests a model of neuroplasticity in form of a fundamental regulatory circle, in which neuronal networks-challenged by cognitive tasks-drift into transient hypoxia, thereby triggering neuronal EPO/EPOR expression.

| S-EPMC7062779 | biostudies-literature

Gamma aminobutyric acid increases erythropoietin overexpression of hypoxia inducible factors in rats

Project description:Gamma aminobutyric acid increases erythropoietin overexpression of hypoxia inducible factors in rats

| PRJNA610051 | ENA

Hypoxia drives HIF2-dependent reversible macrophagecellcycle entry

Project description:Hypoxia drives HIF2-dependent reversible macrophagecellcycle entry

| PRJNA1123255 | ENA

Hippocampal neurons respond to brain activity with functional hypoxia

Project description:Physical activity and cognitive challenge are established non-invasive methods to induce comprehensive brain activation and thereby improve global brain function including mood and emotional well-being in healthy subjects and in patients. However, the mechanisms underlying this experimental and clinical observation and broadly exploited therapeutic tool are still widely obscure. Here we show in the behaving brain that physiological (endogenous) hypoxia is likely a respective lead mechanism, regulating hippocampal plasticity via adaptive gene expression. A refined transgenic approach in mice, utilizing the oxygen-dependent degradation (ODD) domain of HIF-1α fused to CreERT2 recombinase, allows us to demonstrate hypoxic cells in the performing brain under normoxia and motor-cognitive challenge, and spatially map them by light-sheet microscopy, all in comparison to inspiratory hypoxia as strong positive control. We report that a complex motor-cognitive challenge causes hypoxia across essentially all brain areas, with hypoxic neurons particularly abundant in the hippocampus. These data suggest an intriguing model of neuroplasticity, in which a specific task-associated neuronal activity triggers mild hypoxia as a local neuron-specific as well as a brain-wide response, comprising indirectly activated neurons and non-neuronal cells.

2020-11-25 | GSE162079 | GEO

ONECUT2 Drives Neuroendocrine Prostate Cancer Through Hypoxia Signaling

Project description:ONECUT2 Drives Neuroendocrine Prostate Cancer Through Hypoxia Signaling

| PRJNA416257 | ENA

The Long-Form Hypoxia-Inducible Factor 3 Is a Transcription Activator that Regulates Erythropoietin Signaling

Project description:The Long-Form Hypoxia-Inducible Factor 3 Is a Transcription Activator that Regulates Erythropoietin Signaling

| PRJNA529069 | ENA

Gamma aminobutyric acid increases erythropoietin overexpression of hypoxia inducible factors in rats

Project description:Erythropoietin (EPO) is the primary regulator of erythropoiesis in the mammalian fetus and the adult through interaction with erythropoietin receptor (EPOR). Deficiency of EPO induces anemia that is a major cause of death in patients with chronic kidney disease. Thus, development of safe treatment for anemia is an urgent issue. In this study, we investigated the effect of γ-aminobutyric acid (GABA) on serum EPO level and erythropoiesis, and its mechanism was elucidated in rat. GABA significantly (P < 0.05) increased EPO level in serum and expression levels of EPO and EPOR in a dose dependent manner. GABA increased the expression levels of HIF-1 and HIF-2 in a dose dependent manner compared with the negative control; while GABA did not affect the expression of prolyl-hydroxylase domain protein-2α (PHD-2α) gene, an oxygen sensor. GABA supplementation alters energy production pathway resulted in hypoxic condition, which increases EPO level in rat through overexpression of HIF-1 and HIF-2. This study shows a new physiological role of GABA in EPO production and thus GABA could contribute to the prevention of anemia by using alone or in combination with other anemia treating drugs.

2020-03-04 | GSE146299 | GEO

Proteome of Erythropoietin-induced mouse CFU-E cells

Project description:Time-resolved CFU-E proteome was analyzed by time collapsed super-SILAC with erythropoietin-stimulated BaF3-mEpoR proteome as internal heavy standard.

2022-09-28 | PXD004539 | Pride

Hypoxia activates AMPK and drives NLRP3-mediated pyroptosis in periodontitis

Project description:Hypoxia activates AMPK and drives NLRP3-mediated pyroptosis in periodontitis

| PRJNA1092801 | ENA