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Tauroursodeoxycholic acid ameliorates renal injury induced by COL4A3 mutation

ABSTRACT: Tauroursodeoxycholic acid ameliorates renal injury induced by COL4A3 mutation

PROVIDER: PRJNA1087890 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28343902_1.fastq.gz	Fastqsanger.gz
	SRR28343902_2.fastq.gz	Fastqsanger.gz
	SRR28343903_1.fastq.gz	Fastqsanger.gz
	SRR28343903_2.fastq.gz	Fastqsanger.gz
	SRR28343904_1.fastq.gz	Fastqsanger.gz

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Tauroursodeoxycholic acid ameliorates renal injury induced by COL4A3 mutation

Project description:COL4A3/A4/A5 mutations have been identified as critical causes of Alport syndrome and other genetic chronic kidney diseases. However, the underlying pathogenesis remains unclear, and specific treatments are lacking. Here, we constructed a transgenic Alport syndrome mouse model by generating a mutation (Col4a3 p.G799R) identified previously from one large Alport syndrome family into mice. We observed that the mutation caused a pathological decrease in intracellular and secreted collagen IV α3α4α5 heterotrimers. The mutant collagen IV α3 chains abnormally accumulated in the endoplasmic reticulum and exhibited defective secretion, leading to persistent endoplasmic reticulum stress in vivo and in vitro. RNA-seq analysis revealed that the MyD88/p38 MAPK pathway plays key roles in mediating subsequent inflammation and apoptosis signaling activation. Treatment with tauroursodeoxycholic acid, a chemical chaperone drug that functions as an endoplasmic reticulum stress inhibitor, effectively suppressed endoplasmic reticulum stress, promoted secretion of the α3 chains, and inhibited the activation of the MyD88/p38 MAPK pathway. Tauroursodeoxycholic acid treatment significantly improved renal function in vivo. These results partly clarified the pathogenesis of renal injuries associated with Alport syndrome, especially in glomeruli, and suggested that tauroursodeoxycholic acid might be useful for the early clinical treatment of Alport syndrome.

2024-08-28 | GSE261588 | GEO

Activation of GPER1 in macrophage ameliorates UUO-induced renal fibrosis

Project description:Activation of GPER1 in macrophage ameliorates UUO-induced renal fibrosis

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A human integrin-?3 mutation confers major renal developmental defects.

Project description:Integrin-?3 plays a central role in the interplay of cells, morphogens and ECM, required for proper nephrogenesis, thus adding ITGA3 to the list of CAKUT (congenital anomalies of the kidney and urinary tract)-causing genes. we used renal tissue originally obtained from a patient with an ITGA3 mutation and assessed its gene expression profile as compared to controls

2014-12-15 | E-GEOD-54227 | biostudies-arrayexpress

Blockade of TNFα after ischemia reperfusion injury ameliorates renal prognosis

Project description:Recently, acute kidney injury (AKI) is thought to develop a predisposition toward chronic kidney disease. But the detailed mechanism of the disease progression after AKI is unknown. We made two ischemia-reperfusion injury (IRI) mice models, repaired kidney model and atrophic kidney model, and studied the mechanism that kidney after IRI became atrophy. We found that the atrophy kidney model had two peaks of apoptosis 3 and 14 days after IRI, whereas the repaired kidney model had only one apoptosis peak 3 days after IRI. We showed that the second apoptosis is responsible for the kidney atrophy. Moreover, apoptotic ligands, TNFα and FasL were upregulated at the same time of two apoptosis peaks on the atrophic kidney, and blockade of them before IRI prevented kidney from falling into atrophy. Surprisingly, inhibition of the second apoptosis by anti-TNFα antibody protected from renal atrophy. We propose that apoptosis might play a major role in AKI progression and blockade of TNFα after IRI will be a new therapeutic approach for AKI.

2012-08-10 | GSE39766 | GEO

Isoliensinine ameliorates renal injury via the TGF-β1/SMAD2/3 pathway in spontaneously hypertensive rats [kidney tissue]

Project description:Isoliensinine ameliorates renal injury via the TGF-β1/SMAD2/3 pathway in spontaneously hypertensive rats [kidney tissue]

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Isoliensinine ameliorates renal injury via the TGF-β1/SMAD2/3 pathway in spontaneously hypertensive rats [kidney tissue]

Project description:The goals of this study is to compare the differently expressed genes in renal tissues of WKY and SHR with or without isoliensinine treatment. The SHRs (n=12) were randomly divided into 2 groups: SHR, and SHR + isoliensinine (5mg/kg/d) groups (n=6 for each group). WKY rats (n=6) were set as control. Rats in WKY and SHR groups were intragastrically with double distilled water (dd H2O); while rats in SHR + isoliensinine (5mg/kg/d) group were intragastrically with 5mg/kg/d of isoliensinine for 10 weeks. Then the renal tissues were used to identify differentially expressed genes among different groups.

2023-09-20 | GSE225146 | GEO

Intratumoural mutation profiles in clear cell renal cell carcinoma

Project description:Intratumoural mutation profiles in clear cell renal cell carcinoma by targeted sequencing

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Activation of GPER1 in macrophage ameliorates UUO-induced renal fibrosis

Project description:Numerous studies have proven the critical role of macrophages in the renal fibrosis process. Notably, G Protein-coupled Estrogen Receptor 1 (GPER1), a novel estrogen receptor, has been shown to play a ubiquitous role in the regulation of macrophage activities and proinflammatory pathways. However, the precise role of GPER1 in macrophage-mediated renal fibrosis is unknown. In this study, we aimed to investigate the function of macrophage GPER1 in the UUO-induced renal fibrosis model. Compared to vehicle-treated ovariectomized (OVX) female and male UUO models, we observed that G-1 (GPER1 agonist)-treated OVX female and male UUO mice had fewer renal fibrotic lesions and less M1 and M2 macrophage infiltration in the kidney tissues. Conversely, Gper1 deletion in male UUO mice accelerated renal fibrosis and increased inflammation. In vitro studies also revealed that GPER1 activation reduced M0 macrophage polarization towards M1 and M2 phenotypes. The RNA sequencing analysis and immunoblotting indicated that GPER1 activation was primarily involved in downregulating immune pathways activation and inactivating MAPK pathways. Tubular epithelial cells co-cultured with G1-pretreated M1 macrophages exhibited fewer injuries and immune activation. In addition, fibroblasts co-cultured with G1-pretreated M2 macrophages showed downregulated extracellular matrix expression. Overall, this is the first study to demonstrate the effect of GPER1 on macrophage-mediated renal fibrosis via inhibition of M1 and M2 macrophage polarization. These findings indicate that GPER1 may be a promising therapeutic target for the treatment of renal fibrosis.

2023-12-20 | GSE235718 | GEO