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CaMKIIdelta is required for diabetic hyperglycemia but not nephropathy

ABSTRACT: CaMKIIdelta is required for diabetic hyperglycemia but not nephropathy

PROVIDER: PRJNA662598 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12618606.fastq.gz	Fastqsanger.gz
	SRR12618607.fastq.gz	Fastqsanger.gz
	SRR12618608.fastq.gz	Fastqsanger.gz
	SRR12618609.fastq.gz	Fastqsanger.gz
	SRR12618610.fastq.gz	Fastqsanger.gz

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CaMKIIdelta is required for diabetic hyperglycemia but not nephropathy

Project description:Type 2 diabetes is an increasing pandemic health problem and leads to several late diabetic complications of organs including kidney and eye. Lowering elevated blood glucose levels is the typical therapeutic goal in clinical medicine. However, it is possible that hyperglycemia is only a symptom of diabetes but not the correct target to monitor, in order to prevent late diabetic complications. Instead, other diabetes-related alterations could be primary causes for late diabetic complications. Here, we studied the role of CaM Kinase II δ (CaMKIIδ) that is activated through diabetic metabolism. CaMKIIδ is expressed ubiquitously and might therefore affect several different organ systems. We crossed diabetic leptin receptor mutant mice to mice lacking CaMKIIδ globally. Remarkably, CaMKIIδ-deficient diabetic mice did not develop hyperglycemia. As potential underlying mechanisms, we found evidence for improved insulin sensing and increased glucose transport into skeletal muscle. Despite normoglycemia CaMKIIδ-deficient diabetic mice developed the full picture of diabetic nephropathy. In contrast, diabetic retinopathy was prevented. These data challenge the clinical concept of normalizing elevated high glucose levels in diabetes as a causative treatment strategy for late diabetic complications and call for a more detailed analysis of intracellular metabolites in different organs.

2021-09-06 | GSE157739 | GEO

Diabetic nephropathy

Project description:Gene expression profiling in glomeruli from human kidneys with diabetic nephropathy Keywords = Diabetes Keywords = kidney Keywords = glomeruli Keywords: other

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Human PBMCs: Healthy vs Diabetic nephropathy vs ESRD

Project description:Transcriptional profiling of human PBMCs comparing healthy controls, patients with diabetic nephropathy and patients with ESRD. PBMCs were analyzed as they mediate inflammatory injury. Goal was to determine effects of increasing severity of diabetic nephropathy on global PBMC gene expression. Microarray analysis of PBMCs taken from patients with varying degrees of diabetic nephropathy.

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Project description:In order to more accurately and objectively clarify the biological role of lncRNAs in diabetic nephropathy, we detected their expression profiles in renal tissues from patients with diabetic nephropathy.

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Cellular and Molecular Linkage between Diabetic Nephropathy and Diabetic Retinopathy

Project description:Diabetic nephropathy and diabetic retinopathy are related. We used scRNA-seq and RNA-seq to analyze the cellular linkage between them.

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gut microbiome in diabetic nephropathy

Project description:gut microbiome in diabetic nephropathy

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RNA-Seq of Kidney Glomeruli from Type 2 diabetic (db/db) and non-diabetic mice

Project description:We investigated the gene expression profiles of RNA isolated from kidney glomeruli from aged, 25 week old type-2 diabetic (db/db) and non-diabetic mice. In order to investigate the consequences of hyperglycemia on the pathogenesis and progression of diabetic nephropathy Kidney glomeruli from 3 diabetic and 3 non-diabetic, control mice were isolated and RNA purified for RNA-Seq analysis on the Illumina HiSeq 2000. The goal of the project was to generate comprehensive list of noncoding RNA genes differentially regulated between the two conditions in order to identify novel targets for further study.

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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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