Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA126059 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To explore genes and pathways that were differently regulated in the progression of diabetic nephrology in different gender mice, we performed RNA-seq of kidney from BTBRob/ob (diabetic nephrology) mice and wild type (WT) mice. We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 different gender groups.
2023-09-08 | GSE229193 | GEO
Project description:The D6 receptor can bind and internalize inflammatory chemokines without activating intracellular pathways. D6 can reduce tissue inflammation, presumably by scavenging inflammatory chemokines. In diabetic kidney there is extensive inflammation but the possible role of the D6 receptor has never been tested. In this study, we included the renal gene expression dataset generated from whole kidney RNA extraction in diabetic mice with or without D6 gene knockout, their controls are age and sex matched D6 deficient or wild type mice on FVB background. These data are used to analyze the effects of D6 deletion on progression of diabetic nephropathy.
2013-10-10 | GSE51205 | GEO
Project description:In the present study, we aimed to determine the genes involved in inflammatory process of diabetic nephropathy. ICAM-1+/+ and ICAM-1-/- mice aged 8 weeks were divided into four groups: 1) nondiabetic ICAM-1+/+ mice (ND-WT), 2) nondiabetic ICAM-1-/- mice (ND-KO), 3) streptozotocin (STZ)-induced diabetic ICAM-1+/+ mice (DM-WT), and 4) STZ-induced diabetic ICAM-1-/- mice (DM-KO). Three months after the induction of diabetes, total RNA was extracted from each specimen of renal cortex. We examined gene expression profiles of four groups. We identified 193 genes; the ratio of expression level of DM-WT was >2 or <0.5 of that of DM-KO. Of 193 genes, hierarchical clustering identified 33 genes that were significantly upregulated only in DM-WT but not remarkable in ND-WT and ND-KO. Functional annotation of these 33 genes revealed that the significant functions of them were related to the immune or inflammatory process: immune response, response to stimulus, defense response, immune effector process and antigen processing and presentation. These genes contained several inflammatory related genes, such as chemokine (C-X-C motif) ligand 10, chemokine (c-c motif) ligand 12, and chemokine (c-c motif) ligand 8. In this cluster, we focused on cholecystokinin (CCK) because CCK is one of the most up-regulated genes. Real-time RT-PCR revealed that CCK mRNA expression was significantly up-regulated in DM-WT compared with DM-KO. These results suggest that CCK may play a critical role in the progression of diabetic nephropathy by controlling inflammation in diabetic kidney.
2014-10-08 | GSE21390 | GEO
Project description:The dataset contains 72 RNA-seq samples obtained from adult (P150) C57BL/6JCrl mice. Samples are from total heart, liver and kidney tissue. Four different genotypes are included in the data: 1) wild type, 2) transgenic Ciona intestinalis AOX in Rosa26 locus (Szibor et al. 2017, DOI: 10.1242/dmm.027839), 3) respiratory chain complex III deficient Bcs1lp.S78G knock-in mice (a GRACILE syndrome patient mutation, Leveen et al. 2011, DOI: 10.1002/hep.24031) and 4) a cross between the AOX transgenic and Bcs1lp.S78G mice (Rajendran et al. EMBO Mol Med. In press).
2018-11-16 | E-MTAB-7416 | biostudies-arrayexpress
Project description:The D6 receptor can bind and internalize inflammatory chemokines without activating intracellular pathways. D6 can reduce tissue inflammation, presumably by scavenging inflammatory chemokines. In diabetic kidney there is extensive inflammation but the possible role of the D6 receptor has never been tested. In this study, we included the renal gene expression dataset generated from whole kidney RNA extraction in diabetic mice with or without D6 gene knockout, their controls are age and sex matched D6 deficient or wild type mice on FVB background. These data are used to analyze the effects of D6 deletion on progression of diabetic nephropathy. D6 knockout mice were crossing with FVB stain to produce D6 knockout mice in FVB background (D6). Then D6 was crossed with diabetic mice (OVE) to produce D6 defficient diabetic mice (OVE-D6). These mice were followed up for albuminuria from 2 month old, and sacrificied at 6 months for gene expression and renal morphology analysis. 12 kidney samples (3 per group) were used in this gene array study.
2013-10-10 | E-GEOD-51205 | biostudies-arrayexpress
Project description:Mouse E15.5 cortices: Snf2l Ex6 deleted mice versus wild type controls
| PRJNA151063 | ENA
Project description:Diabetic kidney disease remains the leading cause of end-stage renal disease, affecting ~30% of patients with long-standing type 1 and type 2 diabetes, and is characterized by proteinuria and gradual loss of kidney function. There is intense interest in understanding the responses of the many cell types present in the kidney to the diabetic milleu. In this study, we present single cell transcriptomes of renal cortex samples of wild-type and diabetic (C57BL/6-Ins2Akita/J) mice using Drop-Seq.
2018-03-14 | GSE111752 | GEO
Project description:Expression data from kidney in type 2 diabetic db/db mice
| PRJNA344488 | ENA
Project description:RNA-Seq of Kidney Glomeruli from Type 2 diabetic (db/db) and non-diabetic mice
| PRJNA311282 | ENA
Project description:Hepatic transcriptome in wild-type and LXR-deficient mice
| PRJNA167195 | ENA