Accumulation of Acetaldehyde in aldh2.1-/- Zebrafish Causes Increased Retinal Angiogenesis and Impaired Glucose Homeostasis
Ontology highlight
ABSTRACT:
ORGANISM(S): Danio rerio
PROVIDER: GSE189416 | GEO | 2022/09/07
REPOSITORIES: GEO
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Project description:Transcriptome analysis of Lactococcus lactis cultures comparing control non-induced and induced with acetaldehyde
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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
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
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 | GSE76950 | GEO
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2012-07-05 | GSE30424 | GEO
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2012-07-04 | E-GEOD-30424 | biostudies-arrayexpress
Project description:L. lactis cultures: control vs acetaldehyde-induced
| PRJNA616125 | ENA
Project description:Inflammation, including reactive oxygen species and inflammatory cytokines in tissues amplify various post-translational modifications (PTMs) of self-proteins. A number of PTMs have been identified as autoimmune biomarkers in the initiation and progression of Type 1 diabetes (T1D). In this study, we have identified the citrullination of pancreatic glucokinase (GK) as a result of inflammation, triggering autoimmunity and affecting GK biological functions. Glucokinase is expressed in hepatocytes to regulate glycogen synthesis, and in pancreatic beta cells as a glucose sensor to initiate glycolysis and insulin signaling. We identify autoantibodies and autoreactive CD4+ T cells to glucokinase epitopes in the circulation of T1D patients and NOD mice. Finally, citrullination alters GK biologic activity (Km) and suppresses glucose-stimulated insulin secretion. Our studies define glucokinase as a T1D biomarker, providing new insights of how inflammation drives PTMs to create both neoautoantigens and affect beta cell metabolism.
2022-03-17 | PXD028825 | Pride
Project description:Mathematical Definition
symbol/abbreviation
Mathematical symbols
Keq Equilibrium constant
Ki Inhibition constant
Km Affinity constant
v Predicted enzyme activities
Vf Maximal enzyme activities under saturating substrate and activator
conditions, and in the absence of inhibitors
h Hill coefficient
k Rate constant
Abbreviations
ACET Acetaldehyde
ADH Alcohol dehydrogenase
AK Adenylate kinase
ATPcons ATP consuming reactions
bPG 1,3-bisphosphoglycerate
ENO Enolase
ETOHcy Cytoplasmic ethanol
ETOHex Extracellular ethanol
ETOHexp Ethanol transport
GAP Glyceraldehyde 3-phosphate
GAPD Glyceraldehyde 3-phosphate dehydrogenase
GF Glucose facilitator
GK Glucokinase
GLUCcy Cytoplasmic glucose
GLUCex Extracellular glucose
GLUC6P Glucose 6-phosphate
GPD Glucose 6-phosphate dehydrogenase
KDPG 2-keto-3-deoxy-6-phosphogluconate
KDPGA 2-keto-3-deoxy-6-phosphogluconate aldolase
PDC Pyruvate decarboxylase
PEP Phosphoenolpyruvate
PGD 6-phosphogluconate dehydratase
PGK 3-phosphoglycerate kinase
PGL 6-phosphogluconolactonase
PGLACTON 6-phosphogluconolactone
PGLUCONATE 6-phosphogluconate
PGM Phosphoglycerate mutase
P3G 3-phosphoglycerate
P2G 2-phosphoglycerate
PYK Pyruvate kinase
PYR Pyruvate
2020-08-06 | MODEL2008060001 | BioModels
Project description:The model corresponds to the Table 4 and the last column of table 5 of publication (PMID: 24085837, DOI: 10.1099/mic.0.071340-0).
Mathematical Definition
symbol/abbreviation
Mathematical symbols
Keq Equilibrium constant
Ki Inhibition constant
Km Affinity constant
v Predicted enzyme activities
Vf Maximal enzyme activities under saturating substrate and activator
conditions, and in the absence of inhibitors
h Hill coefficient
k Rate constant
Abbreviations
ACET Acetaldehyde
ADH Alcohol dehydrogenase
AK Adenylate kinase
ATPcons ATP consuming reactions
bPG 1,3-bisphosphoglycerate
ENO Enolase
ETOHcy Cytoplasmic ethanol
ETOHex Extracellular ethanol
ETOHexp Ethanol transport
GAP Glyceraldehyde 3-phosphate
GAPD Glyceraldehyde 3-phosphate dehydrogenase
GF Glucose facilitator
GK Glucokinase
GLUCcy Cytoplasmic glucose
GLUCex Extracellular glucose
GLUC6P Glucose 6-phosphate
GPD Glucose 6-phosphate dehydrogenase
KDPG 2-keto-3-deoxy-6-phosphogluconate
KDPGA 2-keto-3-deoxy-6-phosphogluconate aldolase
PDC Pyruvate decarboxylase
PEP Phosphoenolpyruvate
PGD 6-phosphogluconate dehydratase
PGK 3-phosphoglycerate kinase
PGL 6-phosphogluconolactonase
PGLACTON 6-phosphogluconolactone
PGLUCONATE 6-phosphogluconate
PGM Phosphoglycerate mutase
P3G 3-phosphoglycerate
P2G 2-phosphoglycerate
PYK Pyruvate kinase
PYR Pyruvate
2014-09-15 | MODEL1409050001 | BioModels