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NLRP2 promotes proinflammatory and chemotactic responses in proximal tubular epithelial cells

ABSTRACT: NLRP2 promotes proinflammatory and chemotactic responses in proximal tubular epithelial cells

PROVIDER: PRJNA507959 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8271560.fastq.gz	Fastqsanger.gz
	SRR8271561.fastq.gz	Fastqsanger.gz
	SRR8271558.fastq.gz	Fastqsanger.gz
	SRR8271559.fastq.gz	Fastqsanger.gz

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NLRP2 promotes proinflammatory and chemotactic responses in proximal tubular epithelial cells

Project description:In this study, we investigated the functional role of NLRP2 in proximal tubular epithelial cells by overexpressing it in human conditionally immortalized cells obtained from urine of a healthy subject. We found that NLRP2 markedly upregulates proinflammatory and chemotactic responses as well as downregulates interferon-mediated signaling pathways.

2018-12-04 | GSE123247 | GEO

Expression data from proximal tubular cells of proximal tubular cell-specific KAT5 knockout mice

Project description:Isolated proximal tubular cells from proximal tubular cell-specific KAT5 knockout mice for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain the physiological significance of KAT5 in proximal tubular cells.

2021-11-19 | GSE168535 | GEO

Expression data from proximal tubular cells of proximal tubular cell-specific KAT5 knockout mice

Project description:Expression data from proximal tubular cells of proximal tubular cell-specific KAT5 knockout mice

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C-peptide regulates early transcription in rat proximal tubular cells

Project description:C-peptide exerts beneficial effects on glomerular hyperfiltration in type I diabetic patients. As C-peptide localizes to the nucleus, we investigated the transcriptional activities of C-peptide in proximal tubular cells isolated from diabetic rats. Two groups of proximal tubular cells isolated from type I diabetic rats: 1 treated with C-peptide, and 1 untreated. 2-3 replicates per group.

2011-07-26 | E-GEOD-24687 | biostudies-arrayexpress

Proximal tubular transcriptional response to aristolochic acid

Project description:Proximal tubular transcriptional response to aristolochic acid

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Expression data from Stx2-treated human renal proximal tubular epithelial cell (RPTEC)

Project description:Shiga toxin type 2 (Stx2) from Escherichia coli is thought to be a main factor to casue renal dysfunction in Enterohemorrhagic E. coli (EHEC) infection. The renal dysfunction caused by the proximal tubular defects can be detected in the earlier EHEC infection. However, the precise information of gene expression from proximal tubular epithelial cells has yet to be clarified. We performed microarray experiments using Stx2-injected mouse kidney and Stx2-treated human renal proximal tubular epithelial cells (RPTEC), and extracted common genes that were differentially expressed.

2022-01-01 | GSE172466 | GEO

Canagliflozin impact on human renal proximal tubular cells (HK2)

Project description:The impact of canagliflozin on gene expression changes was investigated in human renal proximal tubular cells (HK2) after pre-treatment with high glucose.

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Transcription profiling by array of human renal proximal tubular cell cultures treated with nephrotoxins

Project description:This experiment is designed to investigate common transcriptional alterations in renal proximal tubular cell cultures due to nephrotoxin exposure.

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Transcriptomics of Marburg virus-infected proximal tubular cells

Project description:Transcriptomics of Marburg virus-infected proximal tubular cells

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NLRP2 Regulates Proinflammatory and Antiapoptotic Responses in Proximal Tubular Epithelial Cells.

Project description:Nod-like Receptor Pyrin domain containing proteins (NLRPs) expressed by resident renal cells may contribute to the pathogenesis of multiple renal diseases. Cystinosis is a genetic disorder that affects kidney and particularly proximal tubular epithelial cells (PTEC). Here, we investigated the expression of NLRP family members in human control and cystinotic conditionally immortalized PTEC. Among all the NLRPs tested, we found that NLRP2 is highly expressed in cystinostic PTEC, but not in PTEC from healthy subjects. The NLRP2 overexpression was confirmed in primary PTEC and in kidney biopsies from cystinotic patients. In order to elucidate the role of NLRP2 in PTEC, we stably transfected control PTEC with an NLRP2-containing plasmid. We showed that NLRP2 markedly increases the production of several NF-κB regulated cytokines and chemokines. Accordingly, we demonstrated that NLRP2 interacts with IKKa and positively regulates the DNA-binding activity of p50 and p65 NF-κB, by modulating the p65 NF-κB phosphorylation status in Serine 536. Transcriptome analysis revealed that NLRP2 also upregulates the expression of profibrotic mediators and reduces that of several interferon-inducible genes. Finally, NLRP2 overexpression decreased the apoptotic cell rate. Consistently, silencing of NLRP2 by small-interfering RNA in cystinotic PTEC resulted in a significant decrease in cytokine and chemokine production as well as in an increase in the apoptosis rate. Altogether, our data reveals a previously unrecognized role for NLRP2 in regulating proinflammatory, profibrotic and antiapoptotic responses in PTEC, through NF-κB activation. Moreover, our findings unveil a novel potential mechanism involving NLRP2 overexpression in the pathogenesis of cystinosis.

| S-EPMC6822264 | biostudies-literature

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