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The comparison of gene expression in hematopietic stem cells (HSCs; LSK cells, Lineage-, c-kit+, Sca-1+) from STZ-indued diabetic/nondiabetic mice.

ABSTRACT: To evaluate gene expression of STZ-induced diabetic mice and nondiabetic control mice

ORGANISM(S): Mus musculus

PROVIDER: GSE224690 | GEO | 2023/09/08

REPOSITORIES: GEO

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The analysis of gene expression in hematopietic stem/progenitor cells (HSPCs; LSK cells, Lineage-, c-kit+, Sca-1+) from diabetic/nondiabetic mice.

Project description:To evaluate gene expression of STZ-induced diabetic mice and nondiabetic control mice

2021-05-14 | GSE117088 | GEO

The comparison of gene expression in hematopietic stem cells (HSCs LSK cells, Lineage-, c-kit+, Sca-1+) from STZ-indued diabetic/nondiabetic mice.

Project description:The comparison of gene expression in hematopietic stem cells (HSCs LSK cells, Lineage-, c-kit+, Sca-1+) from STZ-indued diabetic/nondiabetic mice.

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The analysis of gene expression in hematopietic stem/progenitor cells (HSPCs LSK cells, Lineage-, c-kit+, Sca-1+) from diabetic/nondiabetic mice.

Project description:The analysis of gene expression in hematopietic stem/progenitor cells (HSPCs LSK cells, Lineage-, c-kit+, Sca-1+) from diabetic/nondiabetic mice.

| PRJNA481025 | ENA

Liraglutide effect on STZ Mouse Kidney with diabetic nephropathy

Project description:The effect of liraglutide on the kidney proteome in the STZ mouse model compared to healthy and STZ diabetic control groups.

2019-01-18 | PXD003007 | Pride

microRNA sequencing in kidney glomeruli from diabetic and control mice

Project description:identified cluster of microRNAs significantly increased in kidney glomeruli from diabetic mice compared to nondiabetic control mice RNAs from kidney glomeruli from control mice and STZ-injected diabetic mice were extracted.

2016-06-01 | E-GEOD-69718 | biostudies-arrayexpress

N-glyco STZ mouse kidney - N-glycosylation proteome enrichment analysis in kidney reveals differences between diabetic mouse models

Project description:N-glycosylated proteome of STZ diabetic mice with diabetic nephropathy

2016-12-13 | PXD003196 | Pride

Bezafibrate improves insulin sensitivity and metabolic flexibility in STZ-treated diabetic mice

Project description:Bezafibrate (BEZ), a pan activator of peroxisome proliferator-activated receptors (PPARs), is generally used to treat hyperlipidemia. Clinical trials on patients suffering from type 2 diabetes indicated that BEZ also has beneficial effects on glucose metabolism, but the underlying mechanisms remain elusive. Much less is known about the function of BEZ in type 1 diabetes. Here, we show that BEZ treatment markedly improves hyperglycemia, glucose and insulin tolerance in streptozotocin (STZ)-treated mice, an insulin-deficient mouse model of type 1 diabetes presenting with very high blood glucose levels. Furthermore, BEZ-treated mice also exhibited improved metabolic flexibility as well as an enhanced mitochondrial mass and function in the liver. Our data demonstrate a beneficial effect of BEZ treatment on STZ mice reducing diabetes and suggest that BEZ ameliorates impaired glucose metabolism possibly via augmented hepatic mitochondrial performance, improved insulin sensitivity and metabolic flexibility. We performed gene expression microarray analysis on liver tissue derived from streptozotocin-treated mice treated with bezafibrate in addition.

2016-06-29 | E-GEOD-79008 | biostudies-arrayexpress

Bezafibrate improves insulin sensitivity and metabolic flexibility in STZ-treated diabetic mice

2016-06-29 | GSE79008 | GEO

Gene expression profiles of glomerular endothelial cells support their role in the glomerulopathy of diabetic mice

Project description:Endothelial dysfunction promotes the pathogenesis of diabetic nephropathy (DN), which is considered to be an early event in disease progression. However, the molecular changes associated with glomerular endothelial cell (GEC) injury in early DN are not well defined. Most gene expression studies have relied on the indirect assessment of GEC injury from isolated glomeruli or renal cortices. Here, we present transcriptomic analysis of isolated GECs, using streptozotocin-induced diabetic wildtype (STZ-WT) and diabetic eNOS-null (STZ-eNOS−/−) mice as models of mild and advanced DN, respectively. GECs of both models in comparison to their respective nondiabetic controls showed significant alterations in the regulation of apoptosis, oxidative stress, and proliferation. The extent of these changes was greater in STZ-eNOS−/− than in STZ-WT GECs. Additionally, genes in STZ-eNOS−/− GECs indicated further dysregulation in angiogenesis and epigenetic regulation. Moreover, a biphasic change in the number of GECs, characterized by an initial increase and subsequent decrease over time, was observed only in STZ-eNOS−/− mice. This is consistent with an early compensatory angiogenic process followed by increased apoptosis, leading to an overall decrease in GEC survival in DN progression. From the genes altered in angiogenesis in STZ-eNOS−/− GECs, we identified potential candidate genes, Lrg1 and Gpr56, whose function may augment diabetes-induced angiogenesis. Thus, our results support a role for GEC in DN by providing direct evidence for alterations of GEC gene expression and molecular pathways. Candidate genes of specific pathways, such as Lrg1 and Gpr56, can be further explored for potential therapeutic targeting to mitigate the initiation and progression of DN.

2018-12-01 | GSE123177 | GEO

The expression profile of miRNA in the testis of STZ-induced diabetic rats

Project description:The number of patients with diabetes is increasing worldwide. Diabetic testicular damage can cause spermiogenesis disorders and sexual dysfunction. We thus explored the role of miRNAs in diabetic testicular damage, and revealed that they could serve as effective prevention and treatment therapeutic targets.Streptozotocin (STZ) was used to generate a rat model of type 2 diabetes. Rat testicular tissues were used for miRNA sequencing. we identified 19 differentially expressed miRNAs in the testes of diabetic rats.

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