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Mouse kidneys with ischemia-reperfusion injury Human kidneys with acute kidney injury RELA binding sites in primary human proximal tubular cells

ABSTRACT: Mouse kidneys with ischemia-reperfusion injury Human kidneys with acute kidney injury RELA binding sites in primary human proximal tubular cells

PROVIDER: PRJNA1057811 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27367330_1.fastq.gz	Fastqsanger.gz
	SRR27367330_2.fastq.gz	Fastqsanger.gz
	SRR27367331_1.fastq.gz	Fastqsanger.gz
	SRR27367331_2.fastq.gz	Fastqsanger.gz
	SRR27367332_1.fastq.gz	Fastqsanger.gz

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Activation of the YAP/KLF5 transcriptional cascade in renal tubular cells aggravates kidney injury

Project description:The Hippo/YAP pathway plays a critical role in early embryonic kidney development, but its functions in the adult kidney are less well understood. Our previous work has demonstrated that tubular YAP activation induced by double knockout of the upstream Hippo kinases Mst1 and Mst2 (Mst1/2 dKO) promotes tubular injury and renal inflammation under basal conditions. However, the importance of tubular YAP activation remains to be established in injured kidneys in which many other injurious pathways are simultaneously activated. Several secreted factors were found to be increased by YAP in tubular cells, but how the transcriptional network is altered by YAP is largely unknown. Here, we show that tubular YAP was already activated at 6 h after unilateral ureteral obstruction (UUO). Tubular YAP deficiency greatly attenuated tubular cell over-proliferation, tubular injury and renal inflammation induced by UUO or cisplatin. RNA-Seq, ChIP and luciferase assay revealed that YAP promoted the transcription of the transcription factor KLF5 whereas no interaction between YAP and KLF5 was observed. Consistently, the elevated expression of KLF5 and its target genes in Mst1/2 dKO or UUO kidneys was blocked by ablation of Yap in tubular cells. Inhibition of KLF5 prevented tubular cell over-proliferation, tubular injury and renal inflammation in Mst1/2 dKO kidneys. Therefore, our results demonstrate that tubular YAP is a key player in kidney injury. YAP and KLF5 form a transcriptional cascade, in which tubular YAP activation induced by kidney injury promotes KLF5 transcription. Activation of this cascade induces tubular cell over-proliferation, tubular injury and renal inflammation

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Cut and run profiling of RELA binding sites in primary human proximal tubular cells

Project description:We performed cut and run assay to identify RELA binding sites in human primary proximal tubular cells

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Role of Tubular Cpt1a in Aging Murine Kidneys

Project description:To compare the transcriptional profile in aged kidneys lacking tubular Cpt1a with floxed littermate controls.

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Mouse kidneys with ischemia-reperfusion injury; Human kidneys with acute kidney injury; RELA binding sites in primary human proximal tubular cells

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

2024-07-30 | GSE252111 | GEO

Transcription profiling of mouse contralateral kidneys in response to ischemia reperfusion injury

Project description:Current methods to analyze gene expression measure steady-state levels of mRNA. In order to specifically analyze mRNA transcription, a technique has been developed that can be applied in-vivo in intact cells and animals. The technique is referred with the acronym NIAC-NTR (Non Invasive Application and Capture of Newly Transcribed RNA). This method makes use of the cellular pyrimidine salvage pathway and is based on affinity-chromatographic isolation of thiolated mRNA. When combined with data on mRNA steady-state levels, this method is able to assess the relative contributions of mRNA synthesis and degradation/stabilization. It overcomes limitations associated with currently available methods such as mechanistic intervention that disrupts cellular physiology, or the inability to apply the techniques in-vivo. The method was applied to study renal ischemia reperfusion injury, demonstrating its applicability for whole organs in-vivo. Affymetrix GeneChip microarrays were used to detail regulatory mechanisms of mRNA expression and the relative contributions of RNA synthesis and turnover within distinct pathways, and identification of genes expressed at low abundance at the transcriptional level. Experiment Overall Design: The gene expression and regulation program at the RNA level of contralateral mouse kidneys of model IRI-mice was studied. Total RNA, amplified total RNA and specifically enriched newly transcribed RNA was isolated from normal untreated mouse kidneys and from contralateral mouse kidneys of IRI-mice. This experiment allowed detailed regulatory mechanisms in-vivo of mRNA expression and the relative contributions of RNA synthesis and turnover within distinct pathways, and identification of genes expressed at low abundance at the transcriptional level of contralateral kidneys early (3h) after ischemia-reperfusion-injury..

2008-06-15 | E-GEOD-6698 | biostudies-arrayexpress

Role of Tubular Cpt1a in Aging Murine Kidneys

Project description:Role of Tubular Cpt1a in Aging Murine Kidneys

| PRJNA846071 | ENA

Single Cell Chromatin Accessibility Profiling on the mouse kidneys with ischemia-reperfusion injury

Project description:We performed single nucleus ATAC (snATAC-seq) to generate cell-type-specific chromatin accessibility atlas of the mouse kidneys with ischemia-reperfusion injury. The single nucleus RNA-seq of the same samples were previously published (GEO139107)

2024-07-31 | GSE252105 | GEO

A biologic- and chemical-induced rat model of glomerular and tubular injury

Project description:Nonsurgical rodent chronic kidney disease (CKD) models for both glomerular and tubular injuries are currently limited. This study aimed to develop a rat model of CKD by combining anti-Fx1A with N(ω)-nitrophenyl-L-arginine methyl ester (L-NAME) administration. The rats were assigned to groups receiving L-NAME, anti-Fx1A, anti-Fx1A + L-NAME, or vehicle. Renal function, stiffness, injury biomarkers, histopathology and genome-wide transcriptomic changes were evaluated. Protein and renal injury biomarker levels in the urine were elevated in the anti-Fx1A alone and combination groups. Shear wave elastography revealed increased stiffness of the kidneys in all treatment groups. Histopathological evaluation revealed glomerular injury, characterized by enlarged glomeruli with increased hyaline materials in both anti-Fx1A groups and tubular degeneration/regeneration in the renal cortex of all treated groups, with the highest incidence and severity in the combination group. These tubular changes were sometimes accompanied by interstitial mononuclear cell infiltrates and interstitial fibrosis. Proteinuria and mild changes in blood, urine renal injury biomarkers and imaging endpoints were noted in association with these histopathologic changes. The concurrence and higher incidence and/or severity of glomerular and tubular injuries in the combination group indicate that this would be a useful and relevant CKD model suitable for mechanistic, pharmacologic and toxicological investigations.

2024-12-06 | GSE283627 | GEO

Acyloxyacyl Hydrolase Protects against Kidney Injury via Inhibition of Tubular CD74-Macrophage Crosstalk

Project description:Renal fibrosis is the common pathway in the progression of chronic kidney disease (CKD). Acyloxyacyl hydrolase (AOAH) is expressed in various phagocytes and is highly expressed in proximal tubular epithelial cells (PTECs). Research shows that AOAH plays a critical role in infections and chronic inflammatory diseases, although its role in kidney injury is unknown. Here, we found that AOAH deletion led to exacerbated kidney injury and fibrosis after folic acid (FA) administration, which was reversed by overexpression of Aoah in kidneys. ScRNA-seq revealed that Aoah-/- mice exhibited increased subpopulation of CD74+ PTECs, though the percentage of total PTECs were decreased compared to WT mice after FA treatment. Additionally, exacerbated kidney injury and fibrosis seen in Aoah-/- mice was attenuated via administration of methyl ester of (S, R)-3-(4-hydroxyphenyl)-4,5-dihydro-5-isoxazole acetic acid (ISO-1), an inhibitor of macrophage inhibition factor (MIF) and CD74 binding. Finally, AOAH expression was found positively correlated with estimated glomerular filtration rate while negatively correlated with the degree of renal fibrosis in kidneys of CKD patients. Thus, our work indicates that AOAH protects against kidney injury and fibrosis by inhibiting renal tubular epithelial cells CD74 signaling pathways. Targeting kidney AOAH represents a promising strategy to prevent renal fibrosis progression.

2023-12-01 | GSE234090 | GEO

Transcriptional analysis of murine kidneys after caloric restriction and hypoxic preconditioning in an ischemia-reperfusion injury model

Project description:Preconditioning strategies like caloric restriction (CR) and hypoxic preconditioning (HP) show remarkable protective effects in animal models of acute kidney injury (AKI). Since the underlying molecular effects are still not fully understood we performed an experiment directly comparing CR and HP in a murine model of ischemia-reperfusion injury (IRI) of the kidney. 8 to 12-week-old, male C57BL6/J mice were either put to 4 weeks of caloric restriction (70% of normal food intake) or placed in a hypoxic chamber (8%O2) for 3 consecutive days prior to IRI. Whole kidneys were used for transcriptional analysis (RNAseq) before and after ischemia-reperfusion injury to look for common effects of both modes of preconditioning.

2019-12-31 | E-MTAB-7982 | biostudies-arrayexpress

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