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METTL3-Mediated m6A Modification of TIMP2 mRNA Promotes Podocyte Injury in Diabetic Nephropathy [RNA-seq]

ABSTRACT: METTL3-Mediated m6A Modification of TIMP2 mRNA Promotes Podocyte Injury in Diabetic Nephropathy [RNA-seq]

PROVIDER: PRJNA787123 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17167656_1.fastq.gz	Fastqsanger.gz
	SRR17167656_2.fastq.gz	Fastqsanger.gz
	SRR17167657_1.fastq.gz	Fastqsanger.gz
	SRR17167657_2.fastq.gz	Fastqsanger.gz
	SRR17167658_1.fastq.gz	Fastqsanger.gz

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METTL3-Mediated m6A Modification of TIMP2 mRNA Promotes Podocyte Injury in Diabetic Nephropathy [RNA-seq]

Project description:Epigenetic changes present in many physiological and pathological processes. The N6-methyladenosine (m6A) modification is the most common modification in eukaryotic mRNA. However, the role of m6A modification in diabetic nephropathy (DN) is still elusive. Here, the level of m6A modification was significantly upregulated in podocytes stimulated by high glucose (HG), which was caused by elevated levels of METTL3. The results were consistent in the streptozotocin (STZ)-induced experimental model of type 1 diabetes and db/db type 2 diabetes mice. Knocking out METTL3 significantly reduced the inflammation and apoptosis of HG-stimulated podocytes, while its overexpression significantly aggravated these responses. More importantly, silencing METTL3 both in type 1 and type 2 diabetic mice in vivo significantly reduced urinary albumin excretion and histopathological injury. Mechanistically, METTL3 modulated Notch signaling via the m6A modification of its target gene, TIMP2, and exerted pro-inflammatory and pro-apoptotic effects. Moreover, METTL3 enhanced the stability of TIMP2 in an insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2)-dependent manner. In summary, this study suggested that METTL3-mediated m6A modification is an important mechanism of podocyte injury in DN. Targeting m6A through the writer enzyme METTL3 is a potential approach for the treatment of DN.

2024-12-08 | GSE190436 | GEO

Exon Level Expression Profiling of Diabetic Nephropathy

Project description:Transcriptome comparison of glomeruli from kidneys with diabetic nephropathy (DN) and glomeruli from the unaffected portion of tumor nephrectomies. Transcritomics profile of glomeruli in DN patients explored SRGAP2 was strongly associated with proteinuria and involved in podocyte cytoskeleton organization

2018-07-31 | GSE96804 | GEO

Reduction of SIRPα connects podocyte metabolism dysfunction to inflammatory activation via promoting PKM2 nuclear translocation in diabetes nephropathy II

Project description:A central cause of diabetic nephropathy (DN) is podocyte injury. There are many factors causing podocyte injury in DN, such as hyperglycemia, oxidative stress and inflammation. In this study, a signal regulator protein α (SIRPα) was found to play a critical role in regulating podocyte metabolism, oxidative stress and inflammatory.

2024-12-18 | GSE274089 | GEO

Expression data for OVE26 diabetic mouse podocyte

Project description:Podocytes form filtration barrier through foot process around glomerualar basement membrane and selectively permit permeability of molecular smaller than albumin. Diabetes can cause podocyte pathological changes leading to high urine albumin level. Diabetic mouse model OVE26 has extremly high urine albumin and previously studies indicated its podocyte damaged. Here we try to find the key genes change in OVE26 diabetic mouse model podocyte by microarray assay while normal FVB mouse podocyte set as control. Podocyte eGFP transgenic mice were made on FVB background and crossbred to OVE26 diabetic model. Glomeruli isolated from OVE-GFP mice were digested by trypsin into signal cell. Podocytes with GFP were sorting out by FACS.

2012-03-02 | E-GEOD-36209 | biostudies-arrayexpress

Podocyte injury in Fabry nephropathy

Project description:Podocyte injury in Fabry nephropathy

| PRJNA773084 | ENA

METTL3-mediated m<sup>6</sup>A modification of TIMP2 mRNA promotes podocyte injury in diabetic nephropathy.

Project description:Epigenetic changes are present in many physiological and pathological processes. The N6-methyladenosine (m6A) modification is the most common modification in eukaryotic mRNA. However, the role of m6A modification in diabetic nephropathy (DN) remains elusive. Here, we found that m6A modification was significantly upregulated in the kidney of type 1 and type 2 diabetic mice, which was caused by elevated levels of METTL3. Moreover, METTL3 is increased in podocyte of renal biopsy from patients with DN, which is related to renal damage. METTL3 knockout significantly reduced the inflammation and apoptosis in high glucose (HG)-stimulated podocytes, while its overexpression significantly aggravated these responses in vitro. Podocyte-conditional knockout METTL3 significantly alleviated podocyte injury and albuminuria in streptozotocin (STZ)-induced diabetic mice. Therapeutically, silencing METTL3 with adeno-associated virus serotype-9 (AAV9)-shMETTL3 in vivo mitigated albuminuria and histopathological injury in STZ-induced diabetic mice and db/db mice. Mechanistically, METTL3 modulated Notch signaling via the m6A modification of TIMP2 in an insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2)-dependent manner and exerted pro-inflammatory and pro-apoptotic effects. In summary, this study suggested that METTL3-mediated m6A modification is an important mechanism of podocyte injury in DN. Targeting m6A through the writer enzyme METTL3 is a potential approach for the treatment of DN.

| S-EPMC9077313 | biostudies-literature

Novel role of TrkC in diabetic nephropathy and cross-talk of TrkC with insulin-related signaling

Project description:Diabetic nephropathy is a major cause of end-stage renal disease. Kidney podocytes play a central role in the pathogenesis of diabetic nephropathy. With their intercellular contacts they assemble part of the kidney filter. Many molecular mechanisms of the pathogenesis of diabetic nephropathy are not elucidated and targeted therapies are lacking. Nephron-specific TrkCknockout (TrkC-KO) and TrkC overexpressing mice exhibit features of diabetic nephropathy such as enlarged glomeruli with mesangial proliferation, basement membrane thickening, albuminuria and podocyte loss when aging. Insulin-like growth factor 1 receptor (Igf1R)- associated gene expression was regulated in TrkC-KO mice glomeruli by qPCR. Phosphoproteins associated with insulin, erb-b2 receptor tyrosine kinase (Erbb) and Toll-like receptor signaling were enriched in lysates of podocytes treated with the TrkC ligand neurotrophin-3(Nt-3) in a mass spectrometry analysis. Activation of TrkC by Nt-3 resulted in phosphorylation of the Igf1R on activating tyrosine residues in podocytes. Our results identify TrkC to be a potentially targetable mediator of diabetic nephropathy.

2021-09-10 | PXD017960 | Pride

Diabetic nephropathy

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

2004-04-01 | GSE1009 | GEO

Single-Cell Profiling of Diabetic Nephropathy in a Murine Model Reveals Novel CellChat Signatures, Podocyte-to-Parietal Epithelial Cells Crosstalk

Project description:We used scRNA-seq to confirm the rich cellular interactions between podocytes and glomerular parietal epithelial cells in early diabetic nephropathy and to construct a global view of early diabetic nephropathy.

2024-10-31 | GSE216510 | GEO

To investigate how the glycosylation of podocyte proteins changes during diabetic kidney disease

Project description:Podocytes are cells of the visceral epithelium in the kidneys and form a crucial component of the glomerular filtration barrier, contributing to size selectivity and maintaining a massive filtration surface. We are interested in pursuing a microarray analysis to identify the glycosylation-related genes that are modulated in podocytes during insulin and glucose stimulation. As such, we propose to isolate RNA from cultured AB 8/13 human podocyte cell line in their normal state and treated with different concentrations of insulin and glucose. Initially, we would like to analyze 12 samples (Normal control, 2 Starved controls, Insulin experiments 1-4, and glucose experiments 1-5). These experiments would give us information on the gene regulation changes in different healthy and diabetic conditions. In addition to providing possible identification of the unknown proteins involved with diabetic nephropathy, such analysis would provide novel information about early responses by podocytes in response to insulin and glucose level changes in vitro. The results from this analysis will be utilized to focus our research with regard to glycosylation of the proteins in the podocyte slit diaphragm.

2011-10-02 | E-GEOD-32553 | biostudies-arrayexpress

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