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Gene expression profiles of KK.Cg-Ay/J (KKAy) mice and KK-a/a (KKa) mice

ABSTRACT: Gene expression profiles of KK.Cg-Ay/J (KKAy) mice and KK-a/a (KKa) mice

PROVIDER: PRJNA494787 | ENA |

REPOSITORIES: ENA

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Gene expression profiles of KK.Cg-Ay/J (KKAy) mice and KK-a/a (KKa) mice

Project description:The differential gene expression in hepatocytes was compared between the KK.Cg-Ay/J mice and the KK-a/a mice, corresponding to the Diabetic strain and the control. The microarrays were used to screen the candidates supporting to the essential pathogenesis of Type-2 Diabetes in the pre-developing, early and developing stages, corresponding to the 6 weeks, 16 weeks and 42 weeks. To determine the significant biological processes and pathways contributing to development of Diabetic phenotypes in the KKAy mouse, we identified the candidates with the differential gene expression of the livers by comparison of the KKAy and KKa mice. These genes have relationship linkage to construct the networks for mechanistic explanation of the disease.

2018-12-13 | GSE120864 | GEO

DNA methylation profiles of KK.Cg-Ay/J (KKAy) mice and KK-a/a (KKa) mice

Project description:The differential DNA methylation in hepatocytes was compared between the KK.Cg-Ay/J mice and the KK-a/a mice, corresponding to the Diabetic strain and the wild-type known as control. The methylation microarrays were used to support gene expression for screening the candidates susceptibility to the pathogenesis of Type-2 Diabetes in the pre-development, early and development stages, corresponding to the 6, 16 and 42 weeks old. To determine the methylation-dependent biological processes and pathways contributing to development of Diabetic phenotypes in the KKAy mouse, we identified the candidates with the differential DNA methylation levels between the KKAy and KKa mice. The expression of methylation-dependent genes have relationship linkage to construct the networks for mechanistic explanation of the disease.

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Hepatic gene expression profiles in persimmon peel extract administrated KK-Ay mice

Project description:We have shown in a previous study that the intake of persimmon peel (PP) extract altered hepatic gene expression of insulin signaling and enhanced tyrosine phosphorylation of insulin receptors in nonobese type 2 diabetic Goto–Kakizaki rats. We also showed the alteration of gene expression in fatty acid synthesis and metabolism. To evaluate the effect of PP extract on obese diabetic KK-Ay mice, we fed them a diet mixed with 0.1% of the extract for 8 weeks. The plasma total ketone bodies level of the treated mice were significantly lower than that of the untreated mice. The hepatic gene expression profiles of treated mice indicated upregulation of fatty acid biosynthesis-associated gene expression. Hepatic nonesterified palmitic acid content was higher in treated mice than in untreated mice. These results suggest that the intake of PP extract enhances hepatic fatty acid biosynthesis of KK-Ay mice, reducing their plasma total ketone bodies level.

2018-10-01 | GSE67573 | GEO

DNA methylation profiles of KK.Cg-Ay/J (KKAy) mice and KK-a/a (KKa) mice

Project description:DNA methylation profiles of KK.Cg-Ay/J (KKAy) mice and KK-a/a (KKa) mice

| PRJNA494786 | ENA

Gene expression and DNA methylation profiles of KK.Cg-Ay/J (KKAy) mice and KK-a/a (KKa) mice

Project description:Gene expression and DNA methylation profiles of KK.Cg-Ay/J (KKAy) mice and KK-a/a (KKa) mice

| PRJNA494785 | ENA

Glomerular Haematopoietic Prostaglandin D Synthase‐Prostaglandin D2 Axis Contributes to the Periodontitis‐Related Exacerbation of Diabetic Nephropathy in KK‐Ay Mice

Project description:Diabetic nephropathy (DN) is the leading cause of dialysis and is associated with cardiovascular diseases. To prevent the progression of DN, not only glycemic control but also intervention to exacerbating factors such as chronic inflammation and infection. Recent clinical studies have shown the possible association between chronic kidney disease including DN, and periodontitis. However, the causal relationship that periodontitis could contribute to the progression of DN and its molecular mechanisms has not been understood. In the present study, we investigated ligature-induced experimental periodontitis that might exacerbate glomerular pathology in a DN model KK-Ay mice and the underlying molecular mechanisms. KK-Ay mice with experimental periodontitis showed significantly increased urinary albumin to creatinine ratio, and glomerular pathologies such as glomerular size, mesangial expansion area, fibrotic area, and number of CD68-positive leukocytes compared to those without ligatures. RNA-sequencing in the glomeruli revealed that hematopoietic prostaglandin d2 synthase (Hpgds) was the possible factor bridging periodontitis with the progression of DN. We also found that Hpgds expression was significantly upregulated by hyperglycemia and inflammatory stimuli in mesangial cells. Prostaglandin D2 enhanced hyperglycemia-induced collagen expression in mesangial cells and downregulated the tight junction in renal endothelial cells. Lastly, oral administration with an HPGDS inhibitor HQL-79 successfully prevented the progression of DN in KK-Ay mice by experimental periodontitis. Taken together, experimental periodontitis might contribute to the progression of DN via acceleration of glomerular pathology by upregulation of HPGDS in mesangial cells.

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KK-Ay mice gene expression profile

Project description:Mouse gene express was using Mouse Gene 1.0 ST Array.

2017-07-27 | GSE101879 | GEO

Comparison of expression profiles of WT and Nrf2AY/AY mutant macrophages under electrophilic stress agent [ChIP-Seq]

Project description:Nrf2(A502Y) mutant macrophages Nrf2(AY/AY) macrophages were more susceptible to toxicity of xenobiotics. To confirm preferences of binding sequences of Nrf2 and Nrf2A502Y in vivo, we performed ChIP-Seq analyses using an anti-Nrf2 antibody on the DEM-treated peritoneal macrophages derived from Nrf2+/+ and Nrf2AY/AY mice.

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Comparison of expression profiles of WT and Nrf2AY/AY mutant macrophages under electrophilic stress agent [ChIP-Seq]

2016-01-04 | E-GEOD-75175 | biostudies-arrayexpress