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SLAM-ITseq identifies that Nrf2 induces liver regeneration through the pentose phosphate pathway [Larval SLAM-Itseq]

ABSTRACT: SLAM-ITseq identifies that Nrf2 induces liver regeneration through the pentose phosphate pathway [Larval SLAM-Itseq]

PROVIDER: PRJNA962797 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24331618.fastq.gz	Fastqsanger.gz
	SRR24331619.fastq.gz	Fastqsanger.gz
	SRR24331620.fastq.gz	Fastqsanger.gz
	SRR24331621.fastq.gz	Fastqsanger.gz
	SRR24331622.fastq.gz	Fastqsanger.gz

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SLAM-ITseq identifies that Nrf2 induces liver regeneration through the pentose phosphate pathway

Project description:SLAM-ITseq identifies that Nrf2 induces liver regeneration through the pentose phosphate pathway

| PRJNA962794 | ENA

SLAM-ITseq identifies that Nrf2 induces liver regeneration through the pentose phosphate pathway [Larval SLAM-Itseq]

Project description:We investigated the immediate transcriptional changes in hepatocytes following APAP-induced acute liver injury by exposing lf:UPRT zebrafish larvae to DMSO or APAP in the presence of 4TU. We the performed gene expression profiling analysis on total and nascent counts using data obtained from SLAM-ITseq of WT and Nrf2KO animals.

2024-01-13 | GSE230831 | GEO

Transketolase in human Müller cells is critical to resist light stress through the pentose phosphate and NRF2 pathways

Project description:The Pentose Phosphate Pathway (PPP), a metabolic offshoot of the glycolytic pathway, provides protective metabolites and molecules essential for cell redox balance and survival. Transketolase (TKT) is the critical enzyme that controls the extent of “traffic flow” through the PPP. Here, we explored the role of TKT in maintaining the health of the human retina. We found that Müller cells were the primary retinal cell type expressing TKT in the human retina. We further explored the role of TKT in human Müller cells by knocking down its expression in primary cultured Müller cells (huPMCs), isolated from the human retina (11 human donors in total), under lightinduced oxidative stress. TKT knockdown and light stress reduced TKT enzymatic activities and the overall metabolic activities of huPMCs with no detectable cell death. TKT knockdown restrained the PPP traffic flow, reduced the expression of NAD(P)H Quinone Dehydrogenase 1 (NQO1) and impaired the antioxidative response of NRF2 to light stress. TKT knockdown also inhibited overall glucose intake, reduced expression of Dihydrolipoamide dehydrogenase (DLD) and impaired the energy supply of huPMCs. In summary, Müller cell-mediated TKT activity plays a critical protective role in the stressed retina. Knockdown of TKT disrupted the PPP and impaired overall glucose utilisation by huPMCs and rendered huPMCs more vulnerable to light stress by impairing energy supply and antioxidative NRF2 responses.

2022-06-26 | GSE198554 | GEO

A defective pentose phosphate pathway reduces inflammatory macrophage responses during hypercholesterolemia

Project description:Metabolic reprogramming has emerged as a crucial regulator of immune cell activation but how systemic metabolism influences immune cell metabolism and function remains to be investigated. To investigate the effect of dyslipidemia on immune cell metabolism, we performed in-depth transcriptional, metabolic and functional characterization of macrophages isolated from hypercholesterolemic mice. Systemic metabolic changes in such mice alter cellular macrophage metabolism and attenuate inflammatory macrophage responses. In addition to diminished maximal mitochondrial respiration, hypercholesterolemia reduces the LPS-mediated induction of the pentose phosphate pathway (PPP) and the Nrf2-mediated oxidative stress response. Our observation that suppression of the PPP diminishes LPS-induced cytokine secretion supports the notion that this pathway contributes to inflammatory macrophage responses. Overall, this study reveals that systemic and cellular metabolism are strongly interconnected, together dictating macrophage phenotype and function.

2018-10-31 | GSE107412 | GEO

Progesterone increases metabolism via the pentose phosphate pathway in bovine uterine epithelial cells

Project description:During early pregnancy, glucose is essential for the uterine epithelium and the developing embryo. In cows, studies have shown that progesterone increases the secretion of glucose into the uterine lumen. Nevertheless, how progesterone affects glucose metabolism in the uterine epithelium has been sparsely investigated. Therefore, our objective was to investigate how progesterone influences glucose metabolism in immortalized bovine uterine epithelial (BUTE) cells. Progesterone treatment (10 μM) increased glucose consumption. To gain a more global picture of the effects of progesterone, RNAseq was performed after BUTE cells were treated with vehicle (DMSO) or 10 μM for 24 hours. KEGG analysis indicated that progesterone altered genes associated with metabolic pathways and glutathione metabolism. Manually examining genes unique to specific glucose metabolic pathways identified an increase in the rate-limiting enzyme in the pentose phosphate pathway—glucose-6-phosphate dehydrogenase. Functionally, a major product of the pentose phosphate pathway is NADPH, and progesterone treatment increased NADPH concentrations in BUTE cells. In cows, immunohistochemistry confirmed that glucose-6-phosphate dehydrogenase levels were higher in the uterine epithelium in the luteal phase when progesterone concentrations are high. In conclusion, progesterone increased glucose-6-phosphate dehydrogenase expression and metabolism via the pentose phosphate pathway in the bovine uterine epithelium. This metabolism could provide substrates for cell proliferation, molecules to be secreted into the uterine lumen that supports embryonic development, or maintain reduction/oxidation balance in the uterine epithelium.

2024-10-09 | GSE269076 | GEO

Direct comparison of Cdkn2a and p53 loss reveals global transcriptomic differences, including tumor suppressor dependency on pentose phosphate pathway in MPNST

Project description:Malignant Peripheral Nerve Sheath Tumors (MPNSTs) are aggressive and chemo-resistant sarcomas with poor overall survival. Loss of tumor suppressors CDKN2A (~80%) or P53 (~20%) is a signature event in MPNST development. Here, we use CRISPR/Cas9 somatic tumorigenesis mouse models to mechanistically compare CDKN2A and P53 loss transcriptomic and metabolic differences, leading to therapeutic vulnerabilities in MPNSTs. Multi-omic analyses identified the pentose phosphate pathway (PPP) and regulation of NADPH metabolism as critical metabolic vulnerabilities in the CDKN2A-deleted MPNSTs. Disruption of glucose-6-phosphate dehydrogenase (G6PD), the rate-limiting step in the PPP, slowed CDKN2A-deleted MPNST growth, yet sensitized both genotypes of MPNSTs to standard-of-care chemotherapy. Moreover, the redox-regulated transcription factor NRF2 controlled G6PD activity in these tumors. Genomic analysis of patient samples showed a NRF2 gene signature that correlated with tumor transformation, further underscoring this pathway as a therapeutic target. This work identifies the G6PD/NADPH axis as a central metabolic vulnerability in MPNSTs.

2025-08-01 | GSE275277 | GEO

Transketolase in human Müller cells is critical to resist light stress through the pentose phosphate and NRF2 pathways

Project description:Transketolase in human Müller cells is critical to resist light stress through the pentose phosphate and NRF2 pathways

| PRJNA815960 | ENA

Conserved Spermatogonial Gene Networks Couple to Glutathione and Pentose Phosphate Metabolism but not Cysteine Biosynthesis

Project description:Here, gene profiles in rat spermatogonial stem cell lines are compared to publicly available mouse, monkey and human spermatogonial gene profiles. Interestingly, rat spermatogonia expressed metabolic control factors Foxa1, Foxa2 and Foxa3. Germline Foxa2 was enriched in Gfra1Hi and Gfra1Low undifferentiated A-single spermatogonia. Foxa2-bound loci in spermatogonial chromatin were over-represented by conserved stemness genes (Dusp6, Gfra1, Etv5, Rest, Nanos2, Foxp1) that intersect bioinformatically with conserved glutathione/pentose phosphate metabolism genes (Tkt, Gss, Gclc, Gclm, Gpx1, Gpx4, Fth), marking elevated spermatogonial GSH:GSSG. Cystine-uptake and intracellular conversion to cysteine typically couple glutathione biosynthesis to pentose phosphate metabolism. Rat spermatogonia, curiously, displayed poor germline stem cell viability in cystine-containing media, and, like primate spermatogonia, exhibited reduced transsulfuration pathway markers. Exogenous cysteine, cysteine-like mercaptans, somatic testis cells and ferroptosis inhibitors counteracted the cysteine starvation-induced spermatogonial death and stimulated spermatogonial growth factor activity in vitro.

2020-12-17 | GSE163302 | GEO

SLAM-ITseq identifies that Nrf2 induces liver regeneration through the pentose phosphate pathway

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-01-13 | GSE230832 | GEO

A defective pentose phosphate pathway reduces inflammatory macrophage responses during hypercholesterolemia

Project description:A defective pentose phosphate pathway reduces inflammatory macrophage responses during hypercholesterolemia

| PRJNA420032 | ENA