Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA106555 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Diabetic Neuropathy (DN) is a common complication of diabetes. Currently, there is no drug treatment to prevent or slow the development of DN. Rosiglitazone (Rosi) is a potent insulin sensitizer and may also slow the development of DN by a mechanism independent of its effect on hyperglycemia. A two by two design was used to test the effect of Rosi treatment on the development of DN. Streptozotocin-induced diabetic DBA/2J mice were treated with Rosi. DN and oxidative stress were quantified, and gene expression was profiled using the Affymetrix Mouse Genome 430 2.0 microarray platform. An informatics approach identified key regulatory elements activated by Rosi. Diabetic DBA/2J mice developed severe hyperglycemia, DN and elevated oxidative stress. Rosi treatment did not affect hyperglycemia but did reduce oxidative stress and prevented development of thermal hypoalgesia. Two novel transcription factor binding modules were identified that may control genes correlated to changes in DN following Rosi treatment: SP1F_ZBPF and EGRF_EGRF. Rosi treatment reduced oxidative stress and DN independent of its insulin sensitizing effects. Gene expression profiling identified two novel targets activated by Rosi treatment. These targets may be useful in designing drugs with the same efficacy as Rosi in treating DN but with fewer undesirable effects. Keywords: disease and treatment analysis
2008-05-10 | GSE11343 | GEO
Project description:Diabetic Neuropathy (DN) is a common complication of diabetes. Currently, there is no drug treatment to prevent or slow the development of DN. Rosiglitazone (Rosi) is a potent insulin sensitizer and may also slow the development of DN by a mechanism independent of its effect on hyperglycemia. A two by two design was used to test the effect of Rosi treatment on the development of DN. Streptozotocin-induced diabetic DBA/2J mice were treated with Rosi. DN and oxidative stress were quantified, and gene expression was profiled using the Affymetrix Mouse Genome 430 2.0 microarray platform. An informatics approach identified key regulatory elements activated by Rosi. Diabetic DBA/2J mice developed severe hyperglycemia, DN and elevated oxidative stress. Rosi treatment did not affect hyperglycemia but did reduce oxidative stress and prevented development of thermal hypoalgesia. Two novel transcription factor binding modules were identified that may control genes correlated to changes in DN following Rosi treatment: SP1F_ZBPF and EGRF_EGRF. Rosi treatment reduced oxidative stress and DN independent of its insulin sensitizing effects. Gene expression profiling identified two novel targets activated by Rosi treatment. These targets may be useful in designing drugs with the same efficacy as Rosi in treating DN but with fewer undesirable effects. Experiment Overall Design: There were 4 groups: Experiment Overall Design: Control Experiment Overall Design: Control + Rosi Experiment Overall Design: Diabetic (Type 1) Experiment Overall Design: Diabetic + Rosi Experiment Overall Design: Affymetrix chips were run on five mice from each group. One chip (in the Control group) failed quality control measures and was excluded.
2008-06-20 | E-GEOD-11343 | biostudies-arrayexpress
Project description:The type 2 diabetes medication, rosiglitazone, has come under scrutiny for possibly increasing the risk of cardiac disease and death. To investigate the effects of rosiglitazone on the diabetic heart, we performed cardiac transcriptional profiling of a murine model of type 2 diabetes, the C57BL/KLS-leprdb/leprdb (db/db) mouse. We compared cardiac gene expression profiles from three groups: untreated db/db mice (db-c), db/db mice after rosiglitazone treatment (db-t), and non-diabetic db/+ mice. Mice were divided into three groups: Non-diabetic controls (db/+), untreated diabetic controls (db-c), and rosiglitazone-treated diabetic mice (db-t). Whole-heart RNA from five mice from each of the three groups after four months with or without treatment was used for microarray analysis.Universal Reference RNAs for mouse (Stratagene, La Jolla, CA) were purchased as microarray reference controls.
2012-03-28 | E-GEOD-36875 | biostudies-arrayexpress
Project description:Treatment of DBA/2J mice with a combination of L-methionine and valproic acid significantly attenuated progressive hearing loss. We examined gene expression in the whole cochlea of the mice. This study was aimed to detect genes of which change in expression levels were associated with attenuation of progressive hearing loss in the mice. DBA/2J mice at 4 weeks old (untreated_4-weeks, N=5), mice treated with control vehicle (0.1M sodium bicarbonate) for 8 weeks (Control_vehicle_12-weeks, N=5), and mice treated with L-methionine and valproic acid (MET_and_VA_12-weeks, N=6) were analyzed.
2015-04-15 | E-GEOD-62173 | biostudies-arrayexpress
Project description:Mlycd encodes malonyl-CoA decarboxylase (MCD), which is an enzyme that localizes in the cytosolic, mitochondrial, and peroxisomal compartments and catalyzes the conversion of malonyl-CoA into acetyl-CoA. Malonyl-CoA can be converted into malonylcarnitine (C3DC). Patients with an autosomal recessive defect of MCD and MCD KO mice have pronounced elevations of C3DC. Analysis of plasma C3DC levels in the BxD genetic reference population revealed increased levels in BxD strains that harbor the DBA/2J haplotype at the site of the Mlycd gene. RNA sequencing was performed on two samples of DBA/2J mouse livers and two C57BL/6J mouse livers. Decreased expression of Mlycd gene as well as intronic reads in intron 2 were observed in DBA/2J livers. Long-read sequecing of DBA/2J livers in the Mlycd region confirmed an intracisternal A-particle (IAP) retrotransposon in intron 2 of the DBA/2J Mlycd sequence. To confirm the causal nature of the variant, DBA/2J mice with and without the C57BL/6J variant of Mlycd spliced in were tested for products of MCD enzymatic activity, and the C57BL/6J variant was able to rescue the phenotype seen in the DBA/2J mice.
2024-10-26 | GSE186973 | GEO
Project description:The goal of this study was to analyse the effect of a 12 weeks treatment with rosiglitazone on gene expression in adipose tissue of type 2 diabetic patients. Diabetic patients were treated with rosiglitazone, agonist of PPAR gamma, during 12 weeks. Adipose tissue biopsies were taken before and after the treatment.
2018-04-20 | GSE12793 | GEO
Project description:This dataset consists of single-cell RNA-seq (10X) data from disperesed pancreatic islets of healthy and STZ induced diabetic mice. STZ (Sigma) was injected intraperitoneally in 8-week old male C57BLJ/6 mice at 50 mg/kg for five consecutive days. Islets were isolated from healthy mice and STZ diabetic mice after 100 days of either vehicle or drug treatment.
2020-02-20 | GSE128565 | GEO
Project description:We observe morphological changes of retinal microglia during early stages of diabetic retinopathy in STZ-treated mice. Therefore, in this experiment we assess the impact of STZ-induced diabetic retinopathy on retinal microglia transcriptome during early stages of disease.
2023-10-30 | GSE222005 | GEO
Project description:FK1706 potentiated nerve growth factor-induced neurite outgrowth, putatively mediated via FKBP-52 and the Ras/Raf/MAPK signaling pathway. It also improved mechanical allodynia accompanied by the recovery of intraepidermal nerve fiber density in a painful diabetic neuropathy in rats. We analyzed gene expression of the dorsal root ganglia together with measurement of mechanical allodynia in diabetic rats to try to capture the global fingerprint of changes in gene expression associated with FK1706 administration and also to elucidate the putative mechanisms of its neurotrophic activity in vivo. Normal, STZ-treated controls, and STZ + FK1706 groups were used to evaluate gene expression analysis. Dorsal root ganglia from L4 to L6 were collected at the day after 1, 2, and 3 weeks of FK1706 administration, were immediately immersed in RNAlater reagent, and stored as instructed before RNA extraction. Equal amounts of total RNA from five rats were collected for each group.
2011-11-30 | E-GEOD-34000 | biostudies-arrayexpress
Project description:N-glycosylated proteome of STZ diabetic mice with diabetic nephropathy
2016-12-13 | PXD003196 | Pride