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Tnik depletion induces inflammation and apoptosis in injured renal proximal tubule epithelial cells

ABSTRACT: Tnik depletion induces inflammation and apoptosis in injured renal proximal tubule epithelial cells

PROVIDER: PRJNA891715 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21952105_1.fastq.gz	Fastqsanger.gz
	SRR21952105_2.fastq.gz	Fastqsanger.gz
	SRR21952106_1.fastq.gz	Fastqsanger.gz
	SRR21952106_2.fastq.gz	Fastqsanger.gz
	SRR21952107_1.fastq.gz	Fastqsanger.gz

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Tnik depletion induces inflammation and apoptosis in injured renal proximal tubule epithelial cells

Project description:We performed bulk RNA-seq on primary and immortalized human renal proximal tubule epithelial cells (RPTECs) subjected to siRNA mediated TNIK silencing.

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Project description:Freshly isolated rat kidney proximal tubules were subjected for transcript profiling. Three microarray experiments were done to obtain the kidney proxmial tubule transcriptome.

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Effect of GW4064 on primary cultured mouse kidney proximal tubule cells

Project description:Global gene expression in the primary cultured mouse kidney proximal tubule cells treated either DMSO or 1uM GW4064 (a FXR agonist) was compared. Results provide insight into mechanisms underlying effects of FXR activation on gene expression in mouse kidney proximal tubule cells. Male C57/BJ mice aged 6 weeks were sacrificed under anesthesia and kidney proximal tubule cells were cultured until confluent. Cells were treated with either GW4064 (1uM) or equal amount of DMSO and incubated for 24 hours. 4 total RNA samples per group were analyzed and gene expression was compared between the groups.

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VCAM-1 mediates proximal tubule-immune cell cross talk in failed tubule recovery during AKI-to-CKD transition

Project description:Studies in animal models have suggested a linkage between the inflammatory response to injury and subsequent nephron loss during the acute kidney injury (AKI) to chronic kidney disease (CKD) transition. Failure of normal repair during the CKD transition correlates with de novo expression of vascular cell adhesion protein-1 (VCAM-1) by a subset of injured proximal tubule cells. This study identified the role of VCAM-1 expression in promoting the failed repair state. Single-cell transcriptome analysis of patients with AKI and CKD and whole kidney RNA and protein analyses of mouse models of CKD confirmed a marked increase of VCAM-1 expression in the proximal tubules of injured kidneys. In immortalized mouse proximal tubular cells and primary cultured renal cells (PCRCs), VCAM-1 expression was induced by proinflammatory cytokines including tumor necrosis factor (TNF)-α and interleukin (IL)-1β. Analyses of bulk RNA sequencing of TNF-α-treated primary cultured renal cells or pseudo-bulk RNA sequencing of biopsies from Kidney Precision Medicine Project datasets indicated activation of NF-κB and an enrichment of inflammatory response and cell adhesion pathways in VCAM-1-positive cells. Pharmacological inhibition of NF-κB signaling or genetic deletion of myeloid differentiation factor 88 and TIR domain-containing adapter-inducing interferon-β suppressed TNF-α- and IL-1β-induced VCAM-1 expression in vitro. TNF-α stimulation or overexpression of VCAM-1 significantly increased splenocyte adhesion to the mouse proximal tubular monolayer in culture. These results demonstrate that persistence of proinflammatory cytokines after AKI can induce NF-κB-dependent VCAM-1 expression by proximal tubule cells, mediating increased immune cell adhesion to the tubule and thus promoting further tubule injury and greater risk of progression from AKI to CKD.

2024-09-03 | GSE254359 | GEO

Cysteamine-bicalutamide combination therapy corrects proximal tubule phenotype in cystinosis

Project description:Nephropathic cystinosis is a severe monogenic kidney disorder caused by mutations in CTNS, encoding the lysosomal transporter cystinosin, resulting in lysosomal cystine accumulation. The sole treatment, cysteamine, slows down the disease progression, but does not correct the established renal proximal tubulopathy. Here, we developed a new therapeutic strategy by applying omics to expand our knowledge on the complexity of the disease and prioritize drug targets in cystinosis. We identified alpha-ketoglutarate as a potential metabolite to bridge cystinosin loss to autophagy, apoptosis and kidney proximal tubule impairment in cystinosis. This insight combined with a drug screen revealed a bicalutamide-cysteamine combination treatment as a novel dual-target pharmacological approach for the phenotypical correction of cystinotic kidney proximal tubule cells, patient-derived kidney tubuloids and cystinotic zebrafish.

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Transcriptomes of Major Proximal-Tubule Cell-Culture Models

Project description:Purpose:Cultured cell lines are widely used for research in the physiology, pathophysiology, toxicology and pharmacology of the renal proximal tubule. The lines that are most appropriate for a given use depend on the genes expressed.We have used modern RNA-sequencing techniques to identify the gene expression profile of 14 different cell lines plus primary cultures of mouse proximal tubule and compare them to transcriptomes of native kidney proximal tubules. Methods: 14 different proximal tubule cell lines were grown on permeable supports under conditions specific for the respective lines. RNA-Seq followed standard procedures. Results and conclusion: Transcripts expressed in cell lines showed variable match to transcripts selectively expressed in native proximal tubule. Opossum kidney (OK) cells displayed the highest percentage match (45%) with pig kidney cells (LLC-PK1) close behind (39%). Much lower percentage matches were seen for various human lines including HK-2 cells (26%) and lines from rodent kidneys (18-23%).An online resource (https://esbl.nhlbi.nih.gov/JBrowse/KCT/) has been created for interrogation of the data.No cell line closely matched the transcriptome of native proximal tubule cells. However, some of the lines tested are suitable for the study of particular metabolic and transport processes seen in the proximal tubule.

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Project description:Cultured cell lines are widely used for research in the physiology, pathophysiology, toxicology and pharmacology of the renal proximal tubule. The lines that are most appropriate for a given use depend on the genes expressed. New tools for transcriptomic and proteomic profiling using RNA-sequencing (RNA-Seq) and mass spectrometry make it possible to catalog expressed genes in each cell line. This data set is the protoemic data of Rat NRK-52E cell line. We concludeno cell line fully matched the transcriptome of native proximal tubule cells. However, some of the lines tested are suitable for the study of particular metabolic and transport processes seen in the proximal tubule.

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Translational profiling of proximal tubule in fibrotic kidney

Project description:Injury to the proximal tubule plays a central role in the initiation and progression of kidney fibrosis, and rates of chronic kidney disease progresses approximately 50% faster in males compared to females. We applied Translating Ribosome Affinity Purification (TRAP) followed by RNA-sequencing to characterize the cell-specific proximal tubule transcriptional landscape during fibrosis in male vs. female mice.

2019-09-21 | GSE125015 | GEO

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2015-06-26 | GSE70296 | GEO

Single-nuclear transcriptomics reveals a diversity of proximal tubule cell states in a dynamic response to acute kidney injury.

Project description:We performed a mild-to-moderate ischemia reperfusion injury (IRI) to model injury responses reflective of kidney injury in a variety of clinical settings. Single-nuclear RNA-sequencing (snRNA-seq) of genetically labeled injured PTCs at 7-days (“early”) and 28-days (“late”) time points post-IRI identified specific gene and pathway activity in the injury-repair transition. In particular, we identified Vcam1+/Ccl2+ proximal tubule cells at a late injury stage distinguished by marked activation of NF-kB-, TNF- and AP-1-signaling pathways. This population of PTCs showed features of a senescence-associated secretory phenotype but did not exhibit G2/M cell cycle arrest. These pro-inflammatory, pro-fibrotic proximal tubule cells are likely triggers for chronic disease progression.

2021-06-16 | GSE171417 | GEO

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