SOX9 promotes stress-responsive transcription of VGF nerve growth factor inducible gene in renal tubular epithelial cells
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ABSTRACT:
PROVIDER: PRJNA643502 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12125300_1.fastq.gz | Fastqsanger.gz | |||
| SRR12125300_2.fastq.gz | Fastqsanger.gz | |||
| SRR12125301_1.fastq.gz | Fastqsanger.gz | |||
| SRR12125301_2.fastq.gz | Fastqsanger.gz | |||
| SRR12125302_1.fastq.gz | Fastqsanger.gz |
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Project description:Acute kidney injury (AKI) is a common clinical condition associated with diverse etiologies and abrupt loss of renal function. In patients with sepsis, rhabdomyolysis, cancer, as well as cardiovascular disorders, the underlying disease or associated therapeutic interventions can cause hypoxic, cytotoxic, and inflammatory insults to renal tubular epithelial cells (RTECs) resulting in the onset of AKI. To uncover stress-responsive disease-modifying genes, here we have carried out renal transcriptome profiling in three distinct murine models of AKI. We find that Vgf nerve growth factor inducible gene upregulation is a common transcriptional stress response in RTECs to ischemia, cisplatin, and rhabdomyolysis-associated renal injury. The Vgf gene encodes a secretory peptide precursor protein that has critical neuro-endocrine functions; however, its role in the kidneys remains unknown. Our functional studies show that RTEC-specific Vgf gene ablation exacerbates ischemia, cisplatin, and rhabdomyolysis-associated AKI in vivo and cisplatin-induced RTEC cell death in vitro. Importantly, addback experiments showed that aggravation of cisplatin-induced renal injury caused by Vgf gene ablation is partly reversed by TLQP-21, a Vgf-derived peptide. Finally, in vitro and in vivo mechanistic studies showed that injury-induced Vgf upregulation in RTECs is driven by the transcriptional regulator Sox9. These findings identify Vgf as an essential stress-responsive gene and reveal a crucial molecular target of the Sox9 regulated transcriptional program that controls epithelial cell fate during AKI.
2020-09-03 | GSE153625 | GEO
Project description:Acute kidney injury (AKI) is a common clinical condition associated with diverse etiologies and abrupt loss of renal function. In patients with sepsis, rhabdomyolysis, cancer, and cardiovascular disorders, the underlying disease or associated therapeutic interventions can cause hypoxia, cytotoxicity, and inflammatory insults to renal tubular epithelial cells (RTECs), resulting in the onset of AKI. To uncover stress-responsive disease-modifying genes, here we have carried out renal transcriptome profiling in three distinct murine models of AKI. We find that Vgf nerve growth factor inducible gene up-regulation is a common transcriptional stress response in RTECs to ischemia-, cisplatin-, and rhabdomyolysis-associated renal injury. The Vgf gene encodes a secretory peptide precursor protein that has critical neuroendocrine functions; however, its role in the kidneys remains unknown. Our functional studies show that RTEC-specific Vgf gene ablation exacerbates ischemia-, cisplatin-, and rhabdomyolysis-associated AKI in vivo and cisplatin-induced RTEC cell death in vitro Importantly, aggravation of cisplatin-induced renal injury caused by Vgf gene ablation is partly reversed by TLQP-21, a Vgf-derived peptide. Finally, in vitro and in vivo mechanistic studies showed that injury-induced Vgf up-regulation in RTECs is driven by the transcriptional regulator Sox9. These findings reveal a crucial downstream target of the Sox9-directed transcriptional program and identify Vgf as a stress-responsive protective gene in kidney tubular epithelial cells.
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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.
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