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Empagliflozin Ameliorates Aldehyde Dehydrogenase 2 Deficiency-induced Endothelial Dysfunction

ABSTRACT: Empagliflozin Ameliorates Aldehyde Dehydrogenase 2 Deficiency-induced Endothelial Dysfunction

PROVIDER: PRJNA764589 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15970217_1.fastq.gz	Fastqsanger.gz
	SRR15970217_2.fastq.gz	Fastqsanger.gz
	SRR15970218_1.fastq.gz	Fastqsanger.gz
	SRR15970218_2.fastq.gz	Fastqsanger.gz
	SRR15970219_1.fastq.gz	Fastqsanger.gz

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Empagliflozin Ameliorates Aldehyde Dehydrogenase 2 Deficiency-induced Endothelial Dysfunction

Project description:We conducted RNA sequcing of the homozygous and heterozygous of ALDH2*2 by using human induced pluripotent stem cell-derived endothelial cells (hiPSC-ECs)

2023-03-30 | GSE184419 | GEO

Gene expression data from endometrial cancer patient-derived cells (PDCs) treated with aldehyde dehydrogenase inhibitor

Project description:Three lines of PDCs (EnC-A, EnC-B, and EnC-C) were established from endometrial cancer specimens. Aldehyde dehydrogenase (ALDH) inhibition repressed the cell growth with altered gene expression.

2022-02-22 | GSE127239 | GEO

Analysis of tumor cell plasticity in endometrioid carcinoma using cancer stem cell marker aldehyde dehydrogenase (ALDH)

Project description:To investigate the tumor cell plasticity using aldehyde dehydrogenase (ALDH) 1A1 activity, we established two distinct HEC-1B sublines, in which ALDH1A1-high population accelerated such transition and ALDH1A1-high population did not show such acceleration.

2022-11-30 | GSE212889 | GEO

Role of aldehyde dehydrogenase on the metabolic regulation in Clostridium ljungdahlii fermentation

Project description:Clostridium ljungdahlii not only utilizes CO, but also H2 as energy source during autotrophic growth. And C. ljungdahlii also grows in fructose fermentation. In theory, fructose is a more energetically favourable energy source than syngas in the fermentation of C. ljungdahlii. However, C. ljungdahlii grows insufficiently in fructose and produces less acetate and ethanol, compared to syngas fermentation. In this study, C. ljungdahlii wild type and mutants were fermented on fructose. C. ljungdahlii produced less ethanol than the ΔadhE1 mutant and consumed less fructose. The ΔadhE1+2 mutant cannot grow in the syngas fermentation and produced less ethanol among the three strains. The results showed that aldehyde dehydrogenase inactivation led to efficient metabolism in C. ljungdahlii and the bifunctional aldehyde/alcohol dehydrogenases inactivation led to decrease metabolism. Thus, comparative transcriptomes among cells grown on fructose of three strains were performed to investigate gene expression profiles based on three biological replicates.

2023-06-27 | E-MTAB-13020 | biostudies-arrayexpress

Nuclear receptor NHR-49 promotes peroxisome proliferation to compensate for aldehyde dehydrogenase deficiency in C. elegans

Project description:The intracellular level of fatty aldehydes is tightly regulated to minimize the formation of toxic aldehyde adducts of cellular components. Accordingly, deficiency of a fatty aldehyde dehydrogenase FALDH causes the neurologic disorder Sjögren-Larsson syndrome (SLS) in humans. However, cellular responses to unresolved, elevated fatty aldehyde levels are poorly understood. Based on lipidomic and imaging analysis, we report that the loss of endoplasmic reticulum-, mitochondria- and peroxisomes-associated ALH-4, the C. elegans FALDH ortholog, increases fatty aldehyde levels and reduces fat storage. ALH-4 deficiency in the intestine, cell-nonautonomously induces NHR-49/NHR-79-dependent hypodermal peroxisome proliferation. This is accompanied by the upregulation of catalases and fatty acid catabolic enzymes, as indicated by RNA sequencing. Such a response is required to counteract ALH-4 deficiency since alh-4; nhr-49 double mutant animals are not viable. Our work reveals unexpected inter-tissue communication of fatty aldehyde levels, and suggests pharmacological modulation of peroxisome proliferation as a therapeutic strategy for SLS.

2021-06-07 | GSE162792 | GEO

2 Role of aldehyde dehydrogenase on the metabolic regulation in Clostridium ljungdahlii fermentation

Project description:Clostridium ljungdahlii can utilize CO as energy source during autotrophic growth. C. ljungdahlii grows sufficiently in CO and produces ethanol as the main product. In this study, C. ljungdahlii wild type and mutant were fermented on CO. C. ljungdahlii produced more ethanol than the ΔadhE1 mutant. The results showed that aldehyde dehydrogenase inactivation led to inefficient metabolism in C. ljungdahlii. Thus, comparative transcriptomes among cells grown on CO of WT and ΔadhE1 mutant were performed to investigate gene expression profiles based on three biological replicates.

2023-06-27 | E-MTAB-13021 | biostudies-arrayexpress

Progenitor Cell Marker Aldehyde Dehydrogenase 1a3 Defines a Subset of Failing Pancreatic Beta Cells in Diabetic Mice

Project description:Insulin-producing beta cells become dedifferentiated during diabetes progression. An impaired ability to select substrates for oxidative phosphorylation, or metabolic inflexibility, sets the stage for progression from beta cell dysfunction to beta cell dedifferentiation. In this study, we sought to isolate and functionally characterize failing beta cells, as a preliminary step to identify pathways to reverse dedifferentiation. Using various experimental models of diabetes, we found a striking enrichment in the expression of aldehyde dehydrogenase 1 isoform A3 (ALDH+) as beta cells become dedifferentiated. Flow-sorted ALDH+ islet cells demonstrate impaired glucose-induced insulin secretion, are depleted of Foxo1 and MafA, and include a Neurogenin3-positive subset. RNA sequencing analysis demonstrates that ALDH+ cells are characterized by: (i) impaired oxidative phosphorylation and mitochondrial complex I, IV, and V; (ii) activated RICTOR; and (iii) progenitor cell markers. We propose that impaired mitochondrial function marks the progression from metabolic inflexibility to dedifferentiation in the natural history of beta cell failure. RNA-Sequencing analysis of 2 different cell types in 2 different genotype categories.

2016-09-02 | E-GEOD-78966 | biostudies-arrayexpress

Metabolic effects of novel aldehyde dehydrogenase inhibitors (ALDH) inhibitors

Project description:Effect of novel aldehyde dehydrogenase inhibitors. Before an experiment medium was replaced to medium without glucose with addition of labeled glucose on C13. Next, cells were treated with ALDH inhibitors 673 or 773 for 1, 4, or 8 hr (673&773-Jan26)

2017-06-19 | ST000774 | MetabolomicsWorkbench

Aldehyde dehydrogenase activity is necessary for beta cell development and functionality in mice

Project description:Aims/hypothesis Pancreatic beta cells maintain glucose homeostasis and beta cell dysfunction is a major risk factor in developing diabetes. Therefore, understanding the developmental regulatory networks that define a fully functional beta cell is important for elucidating the genetic origins of the disease. Aldehyde dehydrogenase activity has been associated with stem/progenitor cells and we have previously shown that Aldh1b1 is specifically expressed in pancreas progenitor pools. Here we address the hypothesis that Aldh1b1 may regulate the timing of the appearance and eventual functionality of beta cells. Methods We generated an Aldh1b1-knockout mouse line (Aldh1b1tm1lacZ) and used this to study pancreatic development, beta cell functionality and glucose homeostasis in the absence of Aldh1b1 function. Results Differentiation in the developing pancreas of Aldh1b1tm1lacZ null mice was accelerated. Transcriptome analyses of newborn and adult islets showed misregulation of key beta cell transcription factors and genes crucial for beta cell function. Functional analyses showed that glucose-stimulated insulin secretion was severely compromised in islets isolated from null mice. Several key features of beta cell functionality were affected, including control of oxidative stress, glucose sensing, stimulus-coupling secretion and secretory granule biogenesis. As a result of beta cell dysfunction, homozygous mice developed glucose intolerance and age-dependent hyperglycaemia. Conclusions/interpretation These findings show that Aldh1b1 influences the timing of the transition from the pancreas endocrine progenitor to the committed beta cell and demonstrate that changes in the timing of this transition lead to beta cell dysfunction and thus constitute a diabetes risk factor later in life.

2015-07-31 | GSE58025 | GEO

Role of aldehyde dehydrogenase on the metabolic regulation in Clostridium ljungdahlii fermentation

Project description:Role of aldehyde dehydrogenase on the metabolic regulation in Clostridium ljungdahlii fermentation

| PRJEB62861 | ENA