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Metabolic reprogramming in astrocytes prevents neuronal death through a UCHL1/PFKFB3/H4K8la positive feedback loop

ABSTRACT: Metabolic reprogramming in astrocytes prevents neuronal death through a UCHL1/PFKFB3/H4K8la positive feedback loop

PROVIDER: PRJNA1109283 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28962368_1.fastq.gz	Fastqsanger.gz
	SRR28962368_2.fastq.gz	Fastqsanger.gz
	SRR28962369_1.fastq.gz	Fastqsanger.gz
	SRR28962369_2.fastq.gz	Fastqsanger.gz

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Similar Datasets

Metabolic reprogramming in astrocytes prevents neuronal death through a UCHL1/PFKFB3/H4K8la positive feedback loop

Project description:Astrocytic metabolic reprogramming is an adaptation of metabolic patterns to meet increased energy demands, although the role after spinal cord injury (SCI) remains unclear. Analysis of single-cell RNA sequencing (scRNA-seq) data identified an increase in astrocytic glycolysis, while PFKFB3, a key regulator of glycolytic flux, was significantly upregulated following SCI. Loss of PFKFB3 in astrocytes prohibited neuronal energy supply and enhanced neuronal ferroptosis in vitro and inhibited astrogliosis, expanded neuroinflammation, exacerbated neuronal loss, and hindered functional recovery in vivo after SCI. Mechanistically, deubiquitinase UCHL1 plays a crucial role in stabilizing and enhancing PFKFB3 expression by cleaving K48-linked ubiquitin chains. Genetic deletion of Uchl1 inhibited locomotor recovery after SCI by suppression of PFKFB3-induced glycolytic reprogramming in astrocytes. Furthermore, the UCHL1/PFKFB3 axis increased lactate production, leading to enhanced histone lactylation and subsequent transcription of Uchl1 and several genes related to glycolysis, suggesting a glycolysis/H4K8la/UCHL1 positive feedback loop. These findings help to clarify the role of the UCHL1/PFKFB3/H4K8la loop in modulation of astrocytic metabolic reprogramming and reveal a potential target for treatment of SCI.

2025-02-21 | GSE266984 | GEO

Gene expression data of PFKFB3 KD in SMMC7721 cell line

Project description:Overexpression of 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3), a key molecule of glucose metabolism in cytoplasm, was found in various tumors. Emerging evidence suggested that PFKFB3 also located in nucleus and shown regulatory functions other than glycolysis. In this study, we found that PFKFB3 expression is associated with hepatocellular carcinoma (HCC) growth and mainly located in the nucleus of tumor cells. PFKFB3 overexpression was associated with large tumor size, and poor survival of patients with HCC. Knockdown of PFKFB3 inhibited HCC growth, not only by reducing glucose consuming but also damaging DNA repair function leading to G2/M phase arrest and apoptosis. Therefore, we performed a cDNA microarray in PFKFB3 knockdown SMMC7721 cells.

2018-03-01 | GSE106603 | GEO

Effect of PFKFB3 overexpression on A549 in VSV infection.

Project description:To investigate the function PFKFB3 in RNA virus infection, we established PFKFB3 overexpressed A549 cell lines and infected cells with VSV.

2025-08-01 | GSE210288 | GEO

Astrocytes in the mouse suprachiasmatic nuclei respond directly to glucocorticoids feedback

Project description:Astrocytes in the mouse suprachiasmatic nuclei respond directly to glucocorticoids feedback

| PRJNA1005276 | ENA

PFKFB3 inhibits fructose metabolism in pulmonary microvascular endothelial cells

Project description:We hypothesized that PFKFB3 inhibits fructose metabolism in pulmonary microvascular endothelial cells (PMVECs) and found that PFKFB3 knockout cells survive better than wild type cells in fructose-rich media, more so under hypoxia. Our findings indicate that PFKFB3 is a molecular switch that controls glucose versus fructose utilization in glycolysis and help to better understand lung endothelial cell metabolism during respiratory failure.

2023-08-01 | GSE230660 | GEO

Astrocytes in the mouse suprachiasmatic nuclei respond directly to glucocorticoids feedback

Project description:The circadian timing system anticipates daily recurring changes in the environment to synchronize physiology. In mammals, the master pacemaker is the hypothalamic suprachiasmatic nuclei (SCN), which synchronizes “wake” functions by inducing the circadian release of Glucocorticoids (GCs) from the adrenal gland. GCs peak right before the active phase and set the time of peripheral clocks, however, it is still unclear whether the SCN respond to GCs feedback. While GCs influence directly the SCN during the perinatal period, the adult circuit is considered to be resistant to them, suggesting a reduction of GCs-sensitivity along development. To understand this mechanism, we followed the expression of GC receptor (GR) along mouse SCN development with single cell resolution and show that GR is up-regulated in astrocytes as the circuit matures. We provide in vivo and in vitro evidence that the adult SCN stays responsive to circulating GCs through the activation of GR in astrocytes. Astrocytes’ communication is necessary to induce the GC-dependent shift on the SCN clock. Our data provides insight into the development of the SCN and highlight a new role of astrocytes as time-keepers in the adult. This finding might shed light on how the circadian system adapts to jetlag or shift work.

2024-04-10 | GSE240803 | GEO

PFKFB3 activates CAD to enhance de novo pyrimidine synthesis for cell growth

Project description:Aerobic glycolysis, which is also termed the Warburg effect, is one of the aberrant metabolic pathways in highly proliferating cells. Glycolysis provides glycolytic metabolites to support the generation of biomass, such as nucleotides, amino acids, and lipids. To date, no studies have explored interrelationships between glycolysis and other metabolic pathways. Phosphofructokinase-2/fructose-2,6-bisphosphatase 3 (PFKFB3) activates glycolysis by synthesizing fructose-2,6-bisphosphate (F2,6BP), which allosterically activates the rate-limiting enzyme 6-phosphofructo-1-kinase (PFK-1). In this study, we found that PFKFB3 directly interacts with and regulates the phosphorylation of carbamoyl-phosphate synthetase 2, aspartate transcarbamylase, and dihydroorotase (CAD), the enzyme catalyzing the first three steps of de novo pyrimidine synthesis. PFKFB3 inactivation reduced de novo pyrimidine synthesis, RNA and DNA production, and the growth of cancer and proliferative cells. Thus, the glycolytic activator PFKFB3 bridges glycolysis with pyrimidine synthesis, unites both glucose metabolism and nucleic acid metabolism, and contributes to cell proliferation under both physiological and pathological conditions.

2025-06-16 | PXD048755 | Pride

Genome wide analysis of differential gene expression of PFKFB3 under- or overexpression upon inhibition or activation of notch signaling in endothelial cells

Project description:Analysis of gene expression profiles upon PFKFB3 under- or overexpression during inhibition or activation of notch signaling. With this experiment we aimed to identify whether alterations in PFKFB3 could influence the expression pattern of angiogenic genes in conditions that favor a tip- or stalk cell gene signature. Total RNA was collected of human umbilical vein endothelial cells either under- or overexpressing PFKFB3 and/ or have inhibited or activated notch signaling respectively. Cells were harvested 48h after manipulation of PFKFB3 and notch levels.

2013-08-01 | E-GEOD-45750 | biostudies-arrayexpress

Endothelial inhibition of the glycolytic activator PFKFB3 induces tumor vessel normalization, impairs metastasis and improves chemotherapy

Project description:Abnormal tumor vessels promote metastasis and impair chemotherapy. Hence, tumor vessel normalization (TVN) by targeting endothelial cells (ECs) is emerging as anti-cancer treatment. Here, we show that tumor ECs (TECs) have a hyper-glycolytic metabolism, shunting glycolytic intermediates to nucleotide synthesis. EC haplo-deficiency or blockade of the glycolytic activator PFKFB3 did not affect tumor growth, but reduced cancer cell intra- and extravasation and metastasis by normalizing tumor vessels, which improved vessel maturation and perfusion. Mechanistically, PFKFB3 inhibition tightened the vascular barrier by reducing VE-cadherin endocytosis in ECs and rendering glycolytic pericytes more quiescent; it also lowered the expression of cancer cell adhesion molecules in ECs. Additionally, PFKFB3-blockade treatment improved chemotherapy. Considering TEC metabolism for anti-cancer treatment might thus merit further attention.

2016-11-17 | E-MTAB-4842 | biostudies-arrayexpress

Effect of PFKFB3 depletion on gene expression of primary murine vascular smooth muscle cells isolated from c57bl/6

Project description:To investigate the functional role of PFKFB3 in VSMCs osteogenic differentiation, we knockdowned PFKFB3 expression in VSMCs using siRNAs

2023-01-31 | GSE221995 | GEO

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