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Inhibition of BRD4 Attenuates ER Stress-induced Renal Ischemic-Reperfusion Injury

ABSTRACT: Inhibition of BRD4 Attenuates ER Stress-induced Renal Ischemic-Reperfusion Injury

PROVIDER: PRJNA896949 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22142410.fastq.gz	Fastqsanger.gz
	SRR22142411.fastq.gz	Fastqsanger.gz
	SRR22142412.fastq.gz	Fastqsanger.gz
	SRR22142413.fastq.gz	Fastqsanger.gz
	SRR22142414.fastq.gz	Fastqsanger.gz

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Inhibition of BRD4 Attenuates ER Stress-induced Renal Ischemic-Reperfusion Injury

Project description:Renal ischemia-reperfusion injury (IRI) leads to endoplasmic reticulum (ER) stress, thereby initiating the unfolded protein response (UPR). When sustained, this response may trigger the inflammation and tubular cell death that acts to aggravate the damage. Here, we show that knockdown of the BET epigenetic reader BRD4 reduces the expression of ATF4 and XBP1 transcription factors under ER stress activation. BRD4 is recruited to the promoter of these highly acetylated genes, initiating gene transcription. Administration of the BET protein inhibitor, JQ1, one hour after renal damage induced by bilateral IRI, reveals reduced expression of ATF4 and XBP1 genes, low KIM-1 and NGAL levels and recovery of the serum creatinine and blood urea nitrogen levels. To determine the molecular pathways regulated by ATF4 and XBP1, we performed stable knockout of both transcription factors using CRISPR-Cas9 and RNA sequencing. The pathways triggered under ER stress were mainly XBP1-dependent, associated with an adaptive UPR, and partially regulated by JQ1. Meanwhile, treatment with JQ1 downmodulated most of the pathways regulated by ATF4 and related to the pathological processes during exacerbated UPR activation. Thus, BRD4 inhibition could be useful for curbing the maladaptive UPR activation mechanisms, thereby ameliorating the progression of renal disease.

2024-02-15 | GSE217103 | GEO

Inhibition of BRD4 Attenuates ER Stress-induced Renal Ischemic-Reperfusion Injury.

| S-EPMC10929187 | biostudies-literature

small RNA-Seq of rat kidney in a model of ischemic preconditioning/ischemia-reperfusion injury

Project description:Ischemic preconditioning is effective in limiting subsequent ischemic acute kidney injury in experimental models. microRNAs are an important class of post-transcriptional regulator and show promise as biomarkers of kidney injury. An evaluation was performed of the time- and dose-dependent effects of ischemic preconditioning in a rat model of functional (bilateral) ischemia-reperfusion injury. A short, repetitive sequence of ischemic preconditioning resulted in optimal protection from subsequent ischemia-reperfusion injury. A detailed characterization of microRNA expression in ischemic preconditioning/ischemia-reperfusion injury was performed by small RNA-Seq.

2021-12-31 | E-MTAB-9896 | biostudies-arrayexpress

Global transcriptomic profiling of ischemic/reperfusion injury in an in vivo mouse model.

Project description:This SuperSeries is composed of the following subset Series: GSE23160: Global transcriptomic profiling of ischemic/reperfusion injury in an in vivo wild-type mouse model. GSE23162: Global transcriptomic profiling of ischemic/reperfusion injury in an in vivo Gpx1 -/- transgenic mouse model. Refer to individual Series

2011-01-10 | E-GEOD-23163 | biostudies-arrayexpress

Exiqon miRCURY microRNA array of rat kidney in a model of ischemic preconditioning/ischemia-reperfusion injury

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Gene expression profile on ischemic kidneys from wildtype C57BL/10 and TLR4 null C57BL/10ScNJ mice

Project description:TLR4 deficiency attenuates kidney injury after ischemic reperfusion as measured by both renal function and morphology. To better understand the role of TLR4 during the acute kidney injury, we used DNA microarray to identify genes that were differentially expressed on kidneys in wildtype B10 mice and TLR4 null mice during the early stage of injury. A murine ischemic reperfusion injury model was established. After right nephrectomy, the left pedicle was clamped for 23min followed by 4hr reperfusion. Sham mice were used as controls. 6 WT males and 6 TLR4 null males were included with 3 ischemic and 3 shams in each group.

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Global transcriptomic profiling of ischemic/reperfusion injury in an in vivo wild-type mouse model.

Project description:Ischemic stroke triggers severe focal hypoperfusion accompanied with deprivation of oxygen and glucose to the cerebral tissue, together with loss of ATP, depolorization of neurons, elevated extracellular potassium concentration, and subsequently leads to excitotoxicity as well as increased oxidative stress promoting microvascular injury, blood-brain-barrier deregulation, post-ischemic inflammation and eventually the consequential neurological deficit. Although reperfusion of ischemic brain tissue is critical for restoring normal function, it can paradoxically result in secondary damage, called ischemia/reperfusion (I/R) injury. Microarray analysis was performed on the right striatum and cortex (corresponded to infarct area) of post-I/R injured brain tissues of wild-type (WT-MCAO) using Illumina mouse Ref8 V2 genechips. Suture-induced middle cerebral artery occlusion was induced for 2h followed by reperfusion, with tissue extraction taking place 2h, 8h and 24h post-reperfusion (n=4 respectively). Sham controls were included in this study too (n=4 respectively).

2011-01-10 | E-GEOD-23160 | biostudies-arrayexpress

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

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Project description:Restoration of blood flow is the definitive therapy to salvage myocardium following ischemic injury. However, sudden restoration of blood flow to the ischemic myocardium causes ischemia reperfusion injury (IRI). Here, the cardioprotective effect of remote ischemic postconditioning (RPostC) was investigated, based on our in vitro rat model of myocardial IRI. Three groups, including Sham, IRI, and IRI+ RPostC, were utilized for the analysis of Affymetrix Rat Gene 2.0 ST chip.

2019-05-15 | GSE122020 | GEO

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