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ABSTRACT: DEF6 regulates renal ischemia reperfusion injury through suppressing the WWP2 mediated ubiquitination of PARP1

PROVIDER: PRJNA1209416 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31967618_1.fastq.gz	Fastqsanger.gz
	SRR31967618_2.fastq.gz	Fastqsanger.gz
	SRR31967619_1.fastq.gz	Fastqsanger.gz
	SRR31967619_2.fastq.gz	Fastqsanger.gz
	SRR31967620_1.fastq.gz	Fastqsanger.gz

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PARP1 binds and regulates expression of extracellular matrix genes in renal tubular epithelial cells [RNA-Seq]

Project description:PARP1 (Poly adenosine diphosphate ribose polymerase 1) is a ribozyme activated by a broken single-stranded DNA. Recent studies implicate PARP1 not only binds DNA but also be an RNA-binding protein. PARP1 participate in the regulation of renal ischemia-reperfusion injury through binding RNAs, but the mechanism is not clear. Reduced levels of PARP1 led to a significant decrease in cell proliferation and necrosis in the renal ischemia-reperfusion injury cells. In this study, RNA‑seq analysis of the transcriptomes of HK-2 cells with PARP1 knockdown, revealed that genes related extracellular matrix organization and immune response were under global transcriptional regulation.

2022-05-06 | GSE157557 | GEO

DEF6 regulates renal ischemia reperfusion injury through suppressing the WWP2 mediated ubiquitination of PARP1

Project description:Background: Renal ischemia-reperfusion injury (RIRI) stands as an unavoidable complication arising from kidney surgery, profoundly intertwined with its prognosis. The role of differentially expressed in FDCP 6 homolog (DEF6) in RIRI remains elusive, despite its confirmation as a potential therapeutic target for diverse diseases. Here, we investigated the mechanism by which DEF6 regulated RIRI. Methods: RNA sequencing data and IP-MS were used to identify the expression and potential targets of DEF6 through bioinformatics analysis. To elucidate the impact of DEF6 on RIRI, both an in vivo model of RIRI in mice and an in vitro model of kidney cell hypoxia/reoxygenation were established. Biochemical and histological analyses were used to investigate the influence of DEF6 on kidney damage mediated by RIRI. Results: We confirmed that DEF6 was upregulated during RIRI and had a close correlation with RIRI-related inflammation and apoptosis. Moreover, inhibition of DEF6 could mitigate RIRI-induced kidney damage, inflammation, and apoptosis. Through our comprehensive mechanistic investigation, we revealed that DEF6 interacts with poly ADP-ribose polymerase 1 (PARP1) and suppresses the ubiquitination of PARP1. Inhibition of DEF6 resulted in reduced cleaveage of PARP1, leading to a marked suppression of PARP1-mediated apoptosis activation. The aggravation effect on inflammation and apoptosis achieved through DEF6 was nullified by the inhibition of NF-κB and Bax/Bcl2 signaling activation through PARP1 deletion. Conclusions: The findings from our study indicate that DEF6 suppressed the WWP2 mediated ubiquitination of PARP1 and modulates the activation of NF-κB and Bax/Bcl2 pathway, thus involved in RIRI-induced inflammation and apoptosis. These results suggest that DEF6 holds promise as a potential therapeutic target for mitigating RIRI.

2025-01-21 | GSE287205 | GEO

E-GEOD-43671

Project description:Time-Dependent Gene Profiling Indicates the Presence of Different Phases for Ischemia/Reperfusion Injury in Retina

2015-07-10 | E-GEOD-43671 | ExpressionAtlas

RNA microarray of rat kidney treated with or without silicon nano-particles against ischemia reperfusion injury

Project description:RNA microarray was performed to evaluate the efficacy of silicon nano-particles on renal transcriptomes of rats against ischemia reperfusion injury. We compared the transcriptomes of ischemia reperfusion injury model rats with or without oral administration of silicon nano-particles. We also tried to check whether the oral silicon nano-particles intake downregulated the biological processes related to oxidative stress.

2020-02-04 | E-MTAB-8687 | biostudies-arrayexpress

McDougal2017 - Metabolism in ischemic cardiomyocytes

Project description:Heart disease remains the leading cause of death globally. Although reperfusion following myocardial ischemia can prevent death by restoring nutrient flow, ischemia/reperfusion injury can cause significant heart damage. The mechanisms that drive ischemia/reperfusion injury are not well understood; currently, few methods can predict the state of the cardiac muscle cell and its metabolic conditions during ischemia. Here, we explored the energetic sustainability of cardiomyocytes, using a model for cellular metabolism to predict the levels of ATP following hypoxia. We modeled glycolytic metabolism with a system of coupled ordinary differential equations describing the individual metabolic reactions within the cardiomyocyte over time. Reduced oxygen levels and ATP consumption rates were simulated to characterize metabolite responses to ischemia. By tracking biochemical species within the cell, our model enables prediction of the cell’s condition up to the moment of reperfusion. The simulations revealed a distinct transition between energetically sustainable and unsustainable ATP concentrations for various energetic demands. Our model illustrates how even low oxygen concentrations allow the cell to perform essential functions. We found that the oxygen level required for a sustainable level of ATP increases roughly linearly with the ATP consumption rate. An extracellular O2 concentration of ~0.007 mM could supply basic energy needs in non-beating cardiomyocytes, suggesting that increased collateral circulation may provide an important source of oxygen to sustain the cardiomyocyte during extended ischemia. Our model provides a time-dependent framework for studying various intervention strategies to change the outcome of reperfusion.

2024-09-02 | BIOMD0000000961 | BioModels

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Project description:Transcription profiling by RNA-seq of murine hearts at different developmental stages and adult mice with ischemia/reperfusion injury

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2019-10-25 | GSE139318 | GEO

miRNA profiling of urinary exosomes to assess the progression of acute kidney injury

Project description:Using renal ischemia-reperfusion injury as a model of acute kidney injury, we deteremined temporally-released miRNAs released in urinary exosomes during the injury

2019-01-05 | GSE124669 | GEO

Effect of tubular IKKb deletion in acute ischemic kidney injury

Project description:To establish the role of Ikkb during acute kidney injury, we use a mouse line with a specific deletion of Ikkb in the renal tubular system and exposed them to ischemia/reperfusion. Sample collection were done 2 days and 14 days after ischemia/reperfusion.

2022-07-09 | GSE207430 | GEO

The analysis of differential gene expression after remote ischemic preconditioning of renal ischemia reperfusion injury

Project description:To investigate the mechanism by which ischemic preconditioning (IPC) produces tissue tolerance to renal ischemia reperfusion injury in a pig model

2016-09-02 | GSE72646 | GEO

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