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Arctigenin attenuates diabetic kidney disease through the activation of PP2A in podocytes

ABSTRACT: Arctigenin attenuates diabetic kidney disease through the activation of PP2A in podocytes

PROVIDER: PRJNA554786 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9691990.fastq.gz	Fastqsanger.gz
	SRR9692000.fastq.gz	Fastqsanger.gz
	SRR9691991.fastq.gz	Fastqsanger.gz
	SRR9692001.fastq.gz	Fastqsanger.gz
	SRR9691992.fastq.gz	Fastqsanger.gz

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Arctigenin attenuates diabetic kidney disease through the activation of PP2A in podocytes

Project description:Arctigenin (ATG) is a major component of Fructus Arctii, which as a traditional herbal remedy reduced proteinuria in diabetic patients. However, whether ATG specifically provided renoprotection in DKD was not known. Here we report that ATG administration is sufficient to attenuate proteinuria and podocyte injury in mouse models of diabetes. Transcriptomic analysis of diabetic mouse glomeruli showed that cell adhesion and inflammation are two key pathways affected by ATG treatment, and mass spectrometry analysis identified protein phosphatase 2A (PP2A) as one of the top ATG-interacting proteins in renal cells. Enhanced PP2A activity by ATG reduces p65 NF-κB-mediated inflammatory response and high glucose-induced migration in cultured podocytes via its interaction with Drebrin-1. Importantly, podocyte-specific Pp2a deletion in mice exacerbates DKD injury and abrogates the ATG-mediated renoprotection. Collectively, our results clearly demonstrate a renoprotective mechanism of ATG via PP2A activation and establish PP2A as a potential target for DKD progression.

2019-07-17 | GSE134327 | GEO

Arctigenin attenuates diabetic kidney disease through the activation of PP2A in podocytes

2019-11-08 | PXD014976 | Pride

Cyclodextrin protects podocytes in diabetic kidney disease [HumanWG-6 v3.0 array]

Project description:Analysis of gene expression changes in differentiated human podocytes treated with the serum from patients with (DKD+) or without (DKD-) diabetic kidney disease when compared to normal subjects (C). The hypothesis is that the three groups can be distinghed by their differential gene expression pattern. The results obtained revealed important information regarding differences in gene expression in human podocytes treated with the serum from patients with (DKD+) or without (DKD-) diabetic kidney disease when compared to normal subjects (C). Human podocytes were contacted with the serum from patients with diabetes and kidney disease (DKD+) or without kidney disease (DKD-) and compared to normal human podocytes contacted with serum from patients without diabetes (C).

2013-07-11 | E-GEOD-46897 | biostudies-arrayexpress

Cyclodextrin protects podocytes in diabetic kidney disease [HumanHT-12 V4.0 array]

2013-07-13 | E-GEOD-46899 | biostudies-arrayexpress

Cyclodextrin protects podocytes in diabetic kidney disease [HumanHT-12 V4.0 array]

2013-07-13 | GSE46899 | GEO

Cyclodextrin protects podocytes in diabetic kidney disease [HumanWG-6 v3.0 array]

2013-07-11 | GSE46897 | GEO

Mitochondria proteomics of murine kidney podocytes

Project description:To understand how diabetes alters the protein subunits of mitochondrial Electron Transfer Chain (ETC) in the podocytes, we performed a proteomic analysis of mitochondrial proteins isolated from primary kidney podocytes of WT (C57BL/6J background) and Ins2Akita/+ diabetic (C57BL/6J background) mice.

2024-02-08 | PXD041202 | Pride

Mitochondria proteomics of murine kidney podocytes

2024-02-08 | PXD045828 | Pride

Arctigenin attenuates diabetic kidney disease through the activation of PP2A in podocytes.

Project description:Arctigenin (ATG) is a major component of Fructus Arctii, a traditional herbal remedy that reduced proteinuria in diabetic patients. However, whether ATG specifically provides renoprotection in DKD is not known. Here we report that ATG administration is sufficient to attenuate proteinuria and podocyte injury in mouse models of diabetes. Transcriptomic analysis of diabetic mouse glomeruli showed that cell adhesion and inflammation are two key pathways affected by ATG treatment, and mass spectrometry analysis identified protein phosphatase 2 A (PP2A) as one of the top ATG-interacting proteins in renal cells. Enhanced PP2A activity by ATG reduces p65 NF-κB-mediated inflammatory response and high glucose-induced migration in cultured podocytes via interaction with Drebrin-1. Importantly, podocyte-specific Pp2a deletion in mice exacerbates DKD injury and abrogates the ATG-mediated renoprotection. Collectively, our results demonstrate a renoprotective mechanism of ATG via PP2A activation and establish PP2A as a potential target for DKD progression.

| S-EPMC6778111 | biostudies-literature

GPR124 Protects against Podocyte Senescence and Injury in Diabetic Kidney Disease

Project description:Cellular senescence is associated with the progression of diabetic kidney disease (DKD), and accelerated podocyte senescence promotes the pathogenesis of renal damage. We found that GPR124 was reduced in cultured human podocytes treated with high glucose (HG).To further clarify the role of GPR124 in podocytes, we overexpressed GPR124 via plasmid-harboring adenovirus infection. By RNA sequencing analysis of podocytes with different treatment, we observed GPR124 overexpression significantly affected several kinds of cell adhesion.

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