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Effect of interfering Itgb6 gene expression on renal proximal tubular epithelial cells during hypoxia/reoxygenation injury

ABSTRACT: Effect of interfering Itgb6 gene expression on renal proximal tubular epithelial cells during hypoxia/reoxygenation injury

PROVIDER: PRJNA1065895 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27596805_1.fastq.gz	Fastqsanger.gz
	SRR27596805_2.fastq.gz	Fastqsanger.gz
	SRR27596806_1.fastq.gz	Fastqsanger.gz
	SRR27596806_2.fastq.gz	Fastqsanger.gz
	SRR27596807_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

The Role of SOX9 in hypoxia/reoxygenation (H/R) injuried mice primary renal tubular epithelial cells

Project description:The Role of SOX9 in hypoxia/reoxygenation (H/R) injuried mice primary renal tubular epithelial cells Purpose: we performed comparative RNA-seq analyses to identify differentially expressed genes between Knockdown of Sox9 and negtive control in hypoxia/reoxygenation (H/R) injuried mice primary renal tubular epithelial cells. Methods:we grew mouse primary renal tubular epithelial cells to approximately 50% confluence, transfected using EndoFectin™ Max (GeneCopoeia, China) 12h before suffering to H/R injury. H/R was used to mimic IRI in vitro. Briefly, cells were incubated in glucose-free medium in a tri-gas incubator (94% N2, 5% CO2 and 1.0% O2) at 37 °C for 6 hours. Subsequently, cells were incubated in complete medium under normal conditions for 18 hours for reoxygenation. Cells were then collected by 1ml TRIzol (Invitrogen, Carlsbad), and sent to Annoroad Corporation (Beijing, China) for high throughout Illumina NovaSeq 6000 sequencing (GPL24247) (Illumina, San Diego, CA, USA). Results: To determine the possible pathways of Sox9 in protecting mice primary renal tubular epithelial cells from injury, we conduct the transcriptomotic sequencing. After sequence, the clean reads rate of all samples were ≥98%.The quality of the assembled transcriptome is good enough for functional annotation and further analysis. Conclusions: We performed RNA-sequencing (RNA-Seq) on isolated mouse renal tubular epithelial cells of two groups, treated with H/R and transfected with siNC (H/R+siNC group) or siSox9 (H/R+siSox9 group). SOX9-responsive genes showed significant enrichment of the WNT signaling pathway in primary tubular epithelial cells.

2022-12-19 | GSE174811 | GEO

The Role of EGR1 in hypoxia/reoxygenation (H/R) injuried mice primary renal tubular epithelial cells

Project description:The Role of EGR1 in hypoxia/reoxygenation (H/R) injuried mice primary renal tubular epithelial cells Purpose: we performed comparative RNA-seq analyses to identify differentially expressed genes between Knockdown of Egr1 and negtive control in hypoxia/reoxygenation (H/R) injuried mice primary renal tubular epithelial cells. Methods:we grew mouse primary renal tubular epithelial cells to approximately 50% confluence, transfected using EndoFectin™ Max (GeneCopoeia, China). H/R was used to mimic IRI in vitro. Briefly, cells were incubated in glucose-free medium in a tri-gas incubator (94% N2, 5% CO2 and 1.0% O2) at 37 °C for 6 hours. Subsequently, cells were incubated in complete medium under normal conditions for 18 hours for reoxygenation. Cells were then collected by 1ml TRIzol (Invitrogen, Carlsbad), and sent to Annoroad Corporation (Beijing, China) for high throughout Illumina NovaSeq 6000 sequencing (GPL24247) (Illumina, San Diego, CA, USA). Results: To determine the possible pathways and downregulated genes of Egr1 in protecting mice primary renal tubular epithelial cells from injury, we conduct the transcriptomotic sequencing. After sequence, the clean reads rate of all samples were ≥98%.The quality of the assembled transcriptome is good enough for functional annotation and further analysis. Conclusions: We performed RNA-sequencing (RNA-Seq) on isolated mouse renal tubular epithelial cells of 3 groups, negtive control(Sham group) treated with H/R (H/R group) or Egr1 overexpression plasmid (Egr1OV group). Egr1-responsive genes showed significant enrichment in proliferation pathway.

2022-12-19 | GSE174808 | GEO

Effect of interfering Itgb6 gene expression on renal proximal tubular epithelial cells during hypoxia/reoxygenation injury

Project description:Integrin αvβ6 holds promise as a therapeutic target for organ fibrosis, yet targeted therapies are hampered by inflammatory-related side effects. Here, we revealed that upregulated αvβ6 in proximal tubule cells (PTCs) is remarkably positively correlated with renal inflammation both in CKD patients and in murine model of ischemia-reperfusion injury (IRI)-induced renal fibrosis. Knockout of αvβ6 significantly reduced the inflammatory response in IRI kidneys, especially the infiltration of pro-inflammatory macrophages. To delve deeper into the mechanism by which αvβ6 modulates inflammatory response, an unbiased RNA-sequencing of si-NC and si-Itgb6-transfected hypoxic TKPTS cells was performed.

2024-01-18 | GSE253494 | 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

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.

2019-02-27 | GSE106156 | GEO

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

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.

2011-02-01 | E-MEXP-2599 | biostudies-arrayexpress

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

| PRJNA708226 | ENA

Canagliflozin impact on human renal proximal tubular cells (HK2)

Project description:Canagliflozin impact on human renal proximal tubular cells (HK2)

| PRJNA415785 | ENA

Streptozotocin induces renal proximal tubular injury through p53 signaling activation

Project description:Streptozotocin (STZ) is an anti-cancer drug that is primarily used to treat neuroendocrine tumors (NETs) in clinical settings and develop type 1 diabetes rodent models in experimental fields. STZ is incorporated into cells through the glucose transporter, GLUT2, which is primarily expressed in pancreatic β-cells or proximal tubular epithelial cells in the kidney. However, its cytotoxic effects on kidney cells have been underestimated and the underlying mechanisms remain unclear. We herein demonstrated that DNA damage and subsequent p53 signaling were responsible for the development of STZ-induced tubular epithelial injury. We detected tubular epithelial DNA damage in NET patients treated with STZ. Unbiased transcriptomics of tubular epithelial cells in vitro showed the activation of the p53 signaling pathway by STZ. STZ induced DNA damage and activated p53 signaling in vivo in a dose-dependent manner, resulting in reduced membrane transport. The localization of STZ-induced kidney injury was limited to within the kidney cortex, which was independent of blood glucose. The pharmacological inhibition of p53 and sodium-glucose transporter 2 (SGLT2) mitigated STZ-induced epithelial injury. However, the cytotoxic effects of STZ on pancreatic β-cells were preserved in SGLT2 inhibitor-treated mice. The present results demonstrate the strong proximal tubular-specific cytotoxicity of STZ and the underlying mechanisms in vivo, which may be ameliorated by a SGLT2 inhibitor pretreatment. Since the cytotoxic effects of STZ against β-cells were not impaired by dapagliflozin, a pretreatment with a SGLT2 inhibitor has potential as a preventative remedy for kidney injury in NET patients treated with STZ.

2023-06-07 | GSE215337 | GEO

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