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Accumulation of Acetaldehyde in aldh2.1-/- Zebrafish Causes Increased Retinal Angiogenesis and Impaired Glucose Homeostasis

ABSTRACT: Accumulation of Acetaldehyde in aldh2.1-/- Zebrafish Causes Increased Retinal Angiogenesis and Impaired Glucose Homeostasis

PROVIDER: PRJNA782975 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17017805.fastq.gz	Fastqsanger.gz
	SRR17017806.fastq.gz	Fastqsanger.gz
	SRR17017807.fastq.gz	Fastqsanger.gz
	SRR17017808.fastq.gz	Fastqsanger.gz
	SRR17017809.fastq.gz	Fastqsanger.gz

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Accumulation of Acetaldehyde in aldh2.1-/- Zebrafish Causes Increased Retinal Angiogenesis and Impaired Glucose Homeostasis

Project description:In conclusion, the data have identified acetaldehyde as the preferred substrate for Aldh2.1’s detoxification ability. In zebrafish acetaldehyde induces impaired glucose metabolism by blocking gene expression of glucokinase and glucose-6-phosphatase. Moreover, Stress-activated protein Kinases JNK and p38 MAPK were activated by elevated endogenous acetaldehyde leading to increased angiogenesis and vasodilatory effects in aldh2.1-/- zebrafish mutants.

2022-09-07 | GSE189416 | GEO

Accumulation of acetaldehyde in aldh2.1<sup>-/-</sup> zebrafish causes increased retinal angiogenesis and impaired glucose metabolism.

Project description: Not available

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Impaired post-ischemic angiogenesis in rats with chronic kidney disease

Project description:Impaired post-ischemic angiogenesis in rats with chronic kidney disease: underlying changes in ischemia-induced early regulation of gene expression We investigated potential molecular mechanisms underlying impaired angiogenesis by a systematic comparison of early gene expression in response to ischemia in rats with or without CKD

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L. lactis cultures: control vs acetaldehyde-induced

Project description:Transcriptome analysis of Lactococcus lactis cultures comparing control non-induced and induced with acetaldehyde

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Gene expression analysis of MCF12A human breast cultures exposed to ethanol or acetaldehyde [miRNA]

Project description:MCF12A monolayer cultures were exposed to ethanol or acetaldehyde for eiher 1 week or 4 weeks Total RNA samples were assayed for gene expression and for microRNA expression. MicroRNA expression was accomplished using 2 experiments. The first experiment included untreated control, ethanol treated (4 weeks at 2.5 mM) and acetaldehyde treated (4 weeks at 1 mM). The data are presented in order of control1 for the ethanol and acetaldehyde treated samples followed by the ethanol and acetaldehyde treated samples, and then the control2 for the soft agar selected sample followed by the soft agar selected sample. The microRNA names are included in separate columns.

2017-02-10 | GSE76952 | GEO

Adipose Rab10 Knockout Causes Insulin Resistance through Impaired Glucose Uptake

Project description:Insulin action in adipocytes affects whole-body insulin sensitivity. Studies of adipose-specific Glut4 knockout mice have established that adipose Glut4 contributes to the control of systemic glucose homeostasis. Presumably, this reflects a role for Glut4-mediated glucose transport in the regulation of secreted adipokines. In cultured 3T3-L1 adipocytes, Rab10 GTPase is required for insulin-stimulated translocation of Glut4 (Sano et al., 2007). The physiological importance of adipose Rab10 and the significance of its role in the control of Glut4 vesicle trafficking in vivo are unknown. Here we report that adipocytes from adipose-specific Rab10 knockout mice have a ~50% reduction in glucose uptake and Glut4 translocation to the cell surface in response to insulin, demonstrating a role for Rab10 in Glut4 trafficking. Moreover, hyperinsulinemic-euglycemic clamp shows decreased whole-body glucose uptake as well as impaired suppression of hepatic glucose production in adipose Rab10 knockout mice. Thus, fully functional Glut4 vesicle trafficking in adipocytes is critical for maintaining insulin sensitivity. Comparative transcriptome analysis of perigonadal adipose tissue demonstrates significant transcriptional similarities between adipose Rab10 knockout mice and adipose Glut4 knockout mice, consistent with the notion that the phenotypic similarities between the two models are mediated by reduced insulin-stimulated glucose transport into adipocytes. Transcriptome sequencing of perigonadal white adipose tissue

2016-06-30 | E-GEOD-70123 | biostudies-arrayexpress

Gene expression analysis of MCF12A human breast cultures exposed to ethanol or acetaldehyde [4 weeks]

Project description:Alcoholism is associated with breast cancer incidence and progression, and moderate chronic consumption of ethanol is a risk factor. The mechanisms involved in alcohol's oncogenic effects are unknown, but it has been speculated that they may be mediated by acetaldehyde. Here, we use the immortalized normal human epithelial breast cell line MCF-12A to determine whether short- or long-term exposure to ethanol or to acetaldehyde, using in vivo compatible ethanol concentrations, induces their oncogenic transformation and/or the acquisition of epithelial mesenchymal transition (EMT). Cultures of MCF-12A cells were incubated with 25 mM ethanol or 2.5 mM acetaldehyde for 1 week, or with lower concentrations (1.0-2.5 mM for ethanol, 1.0 mM for acetaldehyde) for 4 weeks. In the 4 wk incubation, cells were also tested for anchorage independence, including isolation of soft agar selected cells (SASC) from the 2.5 mM ethanol incubations. Cells were analyzed by immuno-cytofluorescence, flow cytometry, western blotting, DNA microarrays, RT/PCR, and assays for miRs. We found that short-term exposure to ethanol, but not, in general, to acetaldehyde, was associated with transcriptional upregulation of the metallothionein family genes, alcohol metabolism genes, and genes suggesting the initiation of EMT, but without related phenotypic changes. Long-term exposure to the lower concentrations of ethanol or acetaldehyde induced frank EMT changes in the monolayer cultures and in SASC as demonstrated by changes in cellular phenotype and mRNA expression. This suggests that low concentrations of ethanol, with little or no mediation by acetaldehyde, induce EMT and some traits of oncogenic transformation such as anchorage independence in normal breast epithelial cells. MCF12A monolayer cultures were exposed to ethanol or acetaldehyde for either 1 week or 4 weeks. Total RNA samples were assayed for gene expression and for microRNA expression.

2017-02-10 | GSE76951 | GEO

Gene expression analysis of MCF12A human breast cultures exposed to ethanol or acetaldehyde [1 week]

2017-02-10 | GSE76950 | GEO

Indole-3-Acetaldehyde Inhibits Escherichia coli O157:H7 Biofilm Formation by Reducing Curli Formation

Project description:Pathogenic biofilms have been associated with persistent infections due to their high resistance to antimicrobial agents. To identify non-toxic biofilm inhibitors for enterohemorrhagic Escherichia coli O157:H7, indole-3-acetaldehyde was used and reduced E. coli O157:H7 biofilm formation. Global transcriptome analyses revealed that indole-3-acetaldehyde most repressed two curli operons, csgBAC and csgDEFG, and induced tryptophanase (tnaAB) in E. coli O157:H7 biofilm cells. Electron microscopy showed that indole-3-acetaldehyde reduced curli production in E. coli O157:H7. Together, this study shows that Actinomycetales are an important resource of biofilm inhibitors as well as antibiotics.

2012-07-05 | GSE30424 | GEO

Acetaldehyde Induced Cell Damage and Genotoxic Effects by Modulating PI3K/AKT and MAPK/ERK Pathways in Human Lung Epithelial Cells

Project description:Long-term acetaldehyde exposure is associated with cell death, oxidative stress, and DNA damage in lung injury such as chronic obstructive pulmonary disease and respiratory distress syndrome, but the signal transduction mechanism linking key processes remains largely unknown. This study aims to reveal molecular mechanisms of cytotoxicity and genotoxicity induced by acetaldehyde based on human bronchial epithelial cells. Firstly, RNA-seq analysis indicated that differentially expressed genes are most enriched in MAPK/ERK and PI3K/AKT pathways. Secondly, significant up-regulation of four key signaling proteins was confirmed. Subsequently, we found that inhibitors of these pathways could significantly reduce cytotoxicity, oxidative stress, and genotoxicity induced by acetaldehyde. Finally, gene silencing was employed to further validate the importance of these pathways, and toxic effects were more effectively alleviated. Our research suggests that acetaldehyde-induced cell damage and genotoxic effects through PI3K/AKT and MAPK/ERK pathways, provide new insights into toxic mechanisms of acetaldehyde-induced lung injury.

2025-02-21 | GSE289892 | GEO

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