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Activation of RXRα reprograms chromatin accessibility to protect against acute kidney injury [ATAC-seq]

ABSTRACT: Purpose: To explore the differences in chromatin openness of PTCs between MI and SI Methods: Kidney proximal tubules were isolated for ATAC-seq Results: Using an optimized data analysis workflow, we mapped reads to the mouse genome (mm10).

ORGANISM(S): Mus musculus

PROVIDER: GSE197814 | GEO | 2022/11/05

REPOSITORIES: GEO

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Activation of RXRα reprograms chromatin accessibility to protect against acute kidney injury [RNA-seq]

Project description:Purpose: To explore whether the differences in chromatin openness correlate with distinct gene expression in PTCs of MI and SI Methods: Proximal tubules were isolated for RNA-seq Results: Using an optimized data analysis workflow, we mapped reads to the mouse genome (mm10). Approximately 2%-13% of the transcripts showed differential expression within the different groups, with a fold change >= 1.5 and p value <0.05.

2022-11-05 | GSE197812 | GEO

Activation of RXRα reprograms chromatin accessibility to protect against acute kidney injury [H3K27ac ChIP-seq]

Project description:Purpose: To explore the differences in H3K27ac distribution in PTCs after MI and SI Methods: Proximal tubules were isolated for H3K27ac ChIP-seq Results: Using an optimized data analysis workflow, we mapped reads to the mouse genome (mm10). Conclusions: We mapped the chromatin occupancy of H3K27ac.

2022-11-05 | GSE213526 | GEO

Activation of RXRα reprograms chromatin accessibility to protect against acute kidney injury [ChIP-seq]

Project description:Purpose: To explore whether the differences in chromatin occupancy of RXRα correlate with distinct gene expression in PTCs of MI and SI Methods: Proximal tubules were isolated for RXRα ChIP-seq Results: Using an optimized data analysis workflow, we mapped reads to the mouse genome (mm10). Conclusions: We mapped the chromatin occupancy of RXRα.

2022-11-05 | GSE197813 | GEO

Activation of RXRα reprograms chromatin accessibility to protect against acute kidney injury.

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-11-05 | GSE197815 | GEO

Endotoxin preconditioning reprograms S1 tubules and macrophages to protect the kidney

Project description:Preconditioning with a small dose of endotoxin confers unparalleled protection against otherwise lethal models of sepsis. The mechanisms of preconditioning have been investigated extensively in isolated immune cells such as macrophages. However, the role of tissue in mediating the protective response to preconditioning remains unknown. Using the kidney as a model organ, we identify the essential role of the renal epithelial cell in mediating the full expression of protective preconditioning. The protective phenotype is characterized by the clustering of macrophages around S1 segments of proximal tubules, which forms a functional unit mediating protection. To investigate the molecular pathways, we laser microdissected S1 segments from the following: 1) Non-preconditioned mice subjected to single-dose 5 mg/kg lipopolysaccharide (0111:B4, LPS) intraperitoneally for 24 hours. 2) Preconditioned mice subjected to 0.25 mg/kg LPS followed 24 hour later by 5 mg/kg LPS (LPS/LPS). 3) Control mice (saline vehicle).

2017-08-10 | GSE102453 | GEO

Genome-wide profiling of gene expression under electro-acupuncture treatment on MI heart in rats

Project description:Purpose: Acupuncture exerts cardioprotective effects on several types of cardiac injuries, especially myocardial ischemia (MI). In order to elucidate the potential mechanisms, RNA-seq by next generation sequencing was used to identify the rat genome-wide alterations after MI and EA treatment in this study Methods: Adult male Sprague Dawley rats (250-300g) were divided into three groups: Control, MI and electro-acupuncture (EA) groups, myocardium mRNA profiles of rats in each group were generated by deep sequencing,using Illumina Hiseq 2000. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: BurrowsâWheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. Results: Using an optimized data analysis workflow, we mapped about 25 million sequence reads per sample to the mouse genome (UCSC RN4) and identified 121,233, 178,242, 161,880 transcripts in the Control, MI and EA rats with TopHat and Cufflinks workflow respectively. Approximately 32% and 22% of the transcripts showed differential expression between the Control and MI, MI and EA respectively with a fold change â¥2.0. Conclusions: Our results for the first time generated genome-wide gene expression profiles both in the rat MI model and in acupuncture treatment by high throughput sequencing. The optimized data analysis workflows reported here should provide a framework for acupuncture investigations of expression profiles. Myocardium mRNA profiles of Control, MI and EA rats were generated by Hiseq 2000, Control and MI+EA group there were three samples, MI group there were two samples.

2016-03-21 | E-GEOD-54132 | biostudies-arrayexpress

Activation of RXRα reprograms chromatin accessibility to protect against acute kidney injury.

Project description:Activation of RXRα reprograms chromatin accessibility to protect against acute kidney injury.

| PRJNA812327 | ENA

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

Endotoxin Preconditioning Reprograms S1 Tubules and Macrophages to Protect the Kidney.

Project description:Preconditioning with a low dose of endotoxin confers unparalleled protection against otherwise lethal models of sepsis. The mechanisms of preconditioning have been investigated extensively in isolated immune cells such as macrophages. However, the role of tissue in mediating the protective response generated by preconditioning remains unknown. Here, using the kidney as a model organ, we investigated cell type-specific responses to preconditioning. Compared with preadministration of vehicle, endotoxin preconditioning in the cecal ligation and puncture mouse model of sepsis led to significantly enhanced survival and reduced bacterial load in several organs. Furthermore, endotoxin preconditioning reduced serum levels of proinflammatory cytokines, upregulated molecular pathways involved in phagocytosis, and prevented the renal function decline and injury induced in mice by a toxic dose of endotoxin. The protective phenotype involved the clustering of macrophages around S1 segments of proximal tubules, and full renal protection required both macrophages and renal tubular cells. Using unbiased S1 transcriptomic and tissue metabolomic approaches, we identified multiple protective molecules that were operative in preconditioned animals, including molecules involved in antibacterial defense, redox balance, and tissue healing. We conclude that preconditioning reprograms macrophages and tubules to generate a protective environment, in which tissue health is preserved and immunity is controlled yet effective. Endotoxin preconditioning can thus be used as a discovery platform, and understanding the role and participation of both tissue and macrophages will help refine targeted therapies for sepsis.

| S-EPMC5748923 | biostudies-literature

ALKBH5 Induces Fibroblast-to-Myofibroblast Transformation During Hypoxia to Protect Against Cardiac Rupture After Myocardial Infarction

Project description:Objectives: To investigate the role of ALKBH5 in fibroblasts during post-myocardial infarction (MI) repair. Background: N6-methyladenosine (m6A) mRNA modification has been shown to play an important role in cardiovascular diseases. The RNA demethylase, AlkB homolog 5 (ALKBH5), is an m6A "eraser" that is responsible for decreased m6A methylation. However, its role in cardiac fibroblasts during the post-MI healing process remains elusive. Methods: MI was mimicked by permanent left anterior descending artery ligation in global ALKBH5-knockout, ALKBH5-knockin, and fibroblast-specific ALKBH5-knockout mice to study the function of ALKBH5 during post-MI collagen repair. Methylated RNA immunoprecipitation sequencing was performed to explore potential ALKBH5 targets. Results: Dramatic alterations in ALKBH5 expression were observed during the early stage post-MI and in hypoxic fibroblasts. Global ALKBH5 knockin reduced infarct size and improved cardiac function after MI. The global and fibroblast-specific ALKBH5-knockout mice both exhibited low survival rates along with poor collagen repair, impaired cardiac function, and cardiac rupture. Both in vivo and in vitro ALKBH5 loss led to impaired fibroblast activation and decreased collagen deposition. Additionally, hypoxia, but not TGF-β1 or Ang II, upregulated ALKBH5 expression in myofibroblasts in a HIF-1α-dependent transcriptional manner. Mechanistically, ALKBH5 promoted the stability of ErbB4 mRNA and the degradation of ST14 mRNA via m6A demethylation. Fibroblast-specific ErbB4 overexpression ameliorated the impaired fibroblast-to-myofibroblast transformation and poor post-MI repair due to ALKBH5 knockout. Conclusions: Fibroblast ALKBH5 positively regulates post-MI healing via post-transcriptional modification and stabilization of ErbB4 mRNA in an m6A-dependent manner. Targeting ALKBH5/ERBB4 may be a potential therapeutic option for post-MI cardiac rupture.

2023-10-01 | GSE226415 | GEO

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