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Liraglutide effect on STZ Mouse Kidney with diabetic nephropathy

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

INSTRUMENT(S): LTQ Orbitrap Elite

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Kidney

DISEASE(S): Type 2 Diabetes Mellitus,Type 1 Diabetes Mellitus,Diabetic Nephropathy

SUBMITTER: Leena Liljedahl

LAB HEAD: Peter James

PROVIDER: PXD003007 | Pride | 2019-01-18

REPOSITORIES: Pride

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			Action	DRS
	140512_LL_STZ_10_NG_200dil_01_140513182729.RAW	Raw
	140512_LL_STZ_12_NG_200dil_01.RAW	Raw
	140512_LL_STZ_15_NG_200dil_01.RAW	Raw
	140512_LL_STZ_20_NG_200dil_01.RAW	Raw
	140512_LL_STZ_24_NG_200dil_01.RAW	Raw

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Publications

The impact of the glucagon-like peptide 1 receptor agonist liraglutide on the streptozotocin-induced diabetic mouse kidney proteome.

Liljedahl Leena L Pedersen Maiken H MH McGuire James N JN James Peter P

Physiological reports 20190201 4

In diabetes mellitus (DM), the kidneys are exposed to increased levels of hyperglycemia-induced oxidative stress. Elevated amounts of reactive oxygen species (ROS) are believed to provoke ultrastructural changes in kidney tissue and can eventually result in DM late complications such as diabetic nephropathy. While it is reported that glucagon-like peptide 1 receptors (GLP-1R) are present in the kidney vasculature, the effects of GLP-1 on the kidney proteome in DM is not well described. Thus, we ...[more]

PMID: 30806030

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microRNA sequencing in kidney glomeruli from diabetic and control mice

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Delayed activation of host innate immune pathways in streptozotocin-induced diabetic hosts leads to more severe disease during infection with Burkholderia pseudomallei

Project description:The purpose of this study was to develop a comprehensive picture of the STZ-diabetic host transcriptional response during the acute stage of melioidosis and investigate the interplay between the diabetic host response and Burkholderia pseudomallei. To adress this, we compared the transcriptome of infected STZ-diabetic liver and spleen with uninfected STZ-diabetic tissues over an infection period of 42 hr (16 hpi, 24 hpi and 42 hpi, respectively) to identify genes whose expression is altered in response to an acute infection. The microarray experimental design included 3 biological replicates for each time point and both liver and spleen were harvested for RNA extraction. The microarray data from each time point was compared relative to uninfected diabetic mice. In addition, the transcriptome of uninfected STZ-diabetic liver and spleen were also compared with uninfected buffer (sodium citrate) control mice.

2011-12-30 | E-GEOD-28683 | biostudies-arrayexpress

ANRIL regulates multiple molecules of pathogenetic significance in diabetic nephropathy

Project description:Background: Hyperglycemia-induced transcriptional alterations lead to aberrant synthesis of a large number of pathogenetic molecules leading to functional and structural damage to multiple end organs including the kidneys. Diabetic nephropathy (DN) remains a major cause of end stage renal disease. Multiple epigenetic mechanisms, including alteration of long non-coding RNAs (lncRNAs) may play a significant role mediating the cellular transcriptional activities. We have previously shown that lncRNA ANRIL may mediate diabetes associated molecular, functional and structural abnormalities in DN. Here we explored downstream mechanisms of ANRIL alteration in DN. Methods: We used renal cortical tissues from ANRIL knockout (KO) mice and wild type (WT) mice, with or without streptozotocin (STZ) induced diabetes for RNA sequencing. The differentially expressed genes were identified using edgeR and DESeq2 computational methods. KEGG and Reactome pathway analyses and network analyses using STRING and IPA were subsequently performed. Results: Diabetic animals showed hyperglycemia, reduced body weight gain, polyuria and increased urinary albumin. Both albuminuria and polyuria were corrected in the KO diabetic mice. RNA analyses showed Diabetes induced alterations of a large number of transcripts in the wild type (WT) animals. ANRIL knockout (KO) prevented a large number of such alterations. The altered transcripts include metabolic pathways, apoptosis, extracellular matrix protein synthesis and degradation, NFKB related pathways, AGE-RAGE interaction pathways etc. ANRIL KO prevented majority of these pathways. Conclusion: These findings suggest that as ANRIL regulates a large number of molecules of pathogenetic significance, it may potentially be a drug target for DN and other chronic diabetic complications.

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Hepatic gene expression in streptozotocin-induced diabetic mice fed a phloridzin diet

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Hepatic gene expression in streptozotocin-induced diabetic mice fed a phloridzin diet

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Expression data from urinary exosome of diabetic and non-diabetic rats

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