Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A Glo1-methylglyoxal pathway that is perturbed in maternal diabetes regulates embryonic and adult neural stem cell pools in offspring

ABSTRACT: We used microarrays to compare the gene expression profile in cultured primary neurospheres derived from the subventricular zone of adult (2 m.o.) offspring of mothers treated with PBS or methylglyoxal during pregnancy

ORGANISM(S): Mus musculus

PROVIDER: GSE79737 | GEO | 2016/03/31

SECONDARY ACCESSION(S): PRJNA316860

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

A Glo1-methylglyoxal pathway that is perturbed in maternal diabetes regulates embryonic and adult neural stem cell pools in offspring

Project description:We used microarrays to compare the gene expression profile in cultured primary neurospheres derived from the subventricular zone of adult (2 m.o.) offspring of mothers treated with PBS or methylglyoxal during pregnancy Primary neurospheres derived from 2-month-old adult CD1 mice born to mothers treated with PBS or MG twice daily from gestational day 12 until delivery were collected, and total RNA extracted. cDNA was hybridized on Affymetrix Mouse Gene 2.0 ST Array and gene expression was analyzed using Partek software. In total, 3 PBS treated and 3 MG treated mice were used.

2016-03-31 | E-GEOD-79737 | biostudies-arrayexpress

ChIP-chip by array of E. coli MG1655 to analyzed the genome-wide redistribution of RNA polymerase upon methylglyoxal stress

Project description:We have analyzed the genome-wide redistribution of RNA polymerase in E.coli upon methylglyoxal stress. Herefore, we have used ChIP-chip against the beta subunit of RNA polymerase and we have assessed changes in RNA polymerase distribution upon sub-lethal and lethal concentrations of methylglyoxal.

2011-12-15 | E-MTAB-100 | biostudies-arrayexpress

Microarray expression of kidney cortex in adult male rats treated with methylglyoxal vs. controls

Project description:In our study, we investigated the effect of methylglyoxal on metabolic, transcriptomic, metabolomic and proteomic profiles in the context of the development of kidney impairment in an experimental model of metabolic syndrome. Dicarbonyl stress was induced in experimental group by intragastrical administration of methylglyoxal (3x/ week in dose 0.5 mg/kg b.wt.for 4 weeks) in a strain of hereditary hypertriglyceridaemic rats (HHTg). Transcriptome assessment in kidney cortex was performed in 8 male adult rats of experimental group and compared to that of 6 age- and sex- matched rats of control group.

2020-02-08 | E-MTAB-7690 | biostudies-arrayexpress

Microarray expression of white adipose tissue in adult male rats treated with methylglyoxal vs. controls

Project description:In our study, we investigated the effect of methylglyoxal on metabolic, transcriptomic, metabolomic and proteomic profiles in the context of metabolic syndrome in an experimental model. Dicarbonyl stress was induced in experimental group by intragastrical administration of methylglyoxal (3x/ week in dose 0.5 mg/kg b.wt.for 4 weeks) in a strain of hereditary hypertriglyceridaemic rats (HHTg). Transcriptome assessment in white adipose tissue was performed in 7 male adult rats of experimental group and compared to that of 6 age- and sex- matched rats of control group.

2021-04-06 | E-MTAB-9013 | biostudies-arrayexpress

The Glycolytic Metabolite Methylglyoxal Covalently Inactivates the NLRP3 Inflammasome.

Project description:Mass Spectrometry data showing MICA crosslinking of NLRP3 Pyrin cysteines and arginines induced by methylglyoxal (MGO)

2024-08-01 | MSV000095503 | MassIVE

Targeting methylglyoxal in diabetic kidney disease using the novel mitochondria-targeted compound MitoGamide

Project description:Diabetic kidney disease (DKD) remains the number one cause of end-stage renal disease in the western world. Currently there is no treatment to cure diabetes or deal effectively with its complications. In experimental diabetes, mitochondrial dysfunction in the kidney has been widely reported with changes in mitochondrial bioenergetics preceding the development of the renal lesion. Glucose-derived molecules generated during diabetes, known as dicarbonyls, such as methylglyoxal, are thought to impair mitochondrial function and may contribute to the pathogenesis of DKD. Here, we sought to target methylglyoxal within the mitochondria using MitoGamide, the novel mitochondria-targeted dicarbonyl scavenger, in an experimental model of diabetes. Male 6-week-old heterozygous Akita mice (C57BL/6-Ins2-Akita/J) or wildtype littermates were randomized to receive MitoGamide (10mg/kg/day) or vehicle by oral gavage for 16 weeks. MitoGamide did not alter blood glucose control or body composition. Akita mice exhibited hallmarks of DKD including albuminuria, hyperfiltration, glomerulosclerosis and renal fibrosis, however, after 16 weeks of treatment, MitoGamide did not substantially improve the renal phenotype. Complex-I-linked mitochondrial respiration was increased in the kidney of Akita mice which was unaffected by MitoGamide. Exploratory studies using transcriptomics identified that MitoGamide induced changes to olfactory signalling, immune system, respiratory electron transport and post-translational protein modification pathways. These findings indicate that targeting methylglyoxal within the mitochondria using MitoGamide is not a valid therapeutic approach for DKD and that other mitochondrial targets or processes upstream should be the focus of therapy.

2020-10-23 | GSE159882 | GEO

Expression data from neurospheres derived from the neocortex, striatum and subventricular zones of the adult mouse brain

Project description:Differential gene expression profiles of neurospheres derived from different regions of the adult brain. In this dataset, we include data on triplicated biological samples from each of the following brain regions: neocortex, striatum, and subventricular zone. We also include duplicated data on neurospheres derived from the dorsal and ventralforebrain neural tubes and one spinal cord of E14.5 mouse embryos for comparison.

2013-10-01 | GSE49194 | GEO

Profiling of Methylglyoxal Blood Metabolism and Advanced Glycation End-Product Proteome using a Chemical Probe

Project description:Methylglyoxal (MG) is a toxic byproduct of the glycolytic pathway and is quantitatively the most important precursor to advanced glycation end-products (AGEs). Insight into which proteins and in particular their individual modification sites are central to understand the involvement of MG and AGE in diabetes and aging related diseases. Here, we present a method to simultaneously monitor protein AGE formation in biological samples by employing an alkyne-labeled methylglyoxal probe. We apply the method to blood and plasma to demonstrate the impact of blood cell glyoxalase activity on plasma protein AGE formation. We move on to isolate proteins modified by the MG probe and accordingly can present the first general inventory of more than 100 proteins and 300 binding sites of the methylglyoxal probe on plasma as well as erythrocytic proteins.

2019-07-31 | PXD011314 | Pride

Quantitative chemoproteomic profiling of protein crosslinks induced by methylglyoxal

Project description:Quantitative chemoproteomic profiling of protein crosslinks induced by methylglyoxal

2022-01-03 | PXD030688 |

IDA-SWATH proteomic analysis of rat hippocampus upon methylglyoxal treatment

Project description:Diabetes is one of the major risk factors for Alzheimer’s disease (AD) development. The role of elevated levels of glucose, methylglyoxal (MGO), and advanced glycation end products (AGEs) in diabetes in the pathogenesis of the AD is not well understood. In this pursuit, we studied the role of methylglyoxal in the pathogenesis of AD in rat models. The elevated plus-maze (EPM) behavioural study indicated that MGO induces anxiety. Treatment of telmisartan (RAGE expression inhibitor) and aminoguanidine (MGO quencher) attenuated MGO induced anxiety. Further, hippocampal proteomics demonstrated that MGO treated rats differentially regulate proteins involved in calcium homeostasis, mitochondrial functioning, and apoptosis which may affect neurotransmission and neuronal plasticity. Hippocampal tau phosphorylation level was increased in MGO treated rats which was reduced in presence in aminoguanidine and telmisartan. Plasma fructosamine level was increased upon MGO treatment. Hippocampal histochemistry showed vascular degeneration and neuronal loss upon MGO treatment. This study provides mechanistic insight into the role of MGO in the diabetes-associated development of AD.

2024-01-26 | PXD037673 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data