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Acute Kidney Injury Transcriptional Profiles: Single Cell RNA Sequencing reveals Injury induced Renal Developmental program reactivation and Lineage Infidelity in adult kidney

ABSTRACT: Acute Kidney Injury Transcriptional Profiles: Single Cell RNA Sequencing reveals Injury induced Renal Developmental program reactivation and Lineage Infidelity in adult kidney

PROVIDER: PRJNA579998 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10356400.fastq.gz	Fastqsanger.gz
	SRR10356401.fastq.gz	Fastqsanger.gz
	SRR10356402.fastq.gz	Fastqsanger.gz
	SRR10356403.fastq.gz	Fastqsanger.gz
	SRR10356404.fastq.gz	Fastqsanger.gz

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Acute Kidney Injury Transcriptional Profiles: Single Cell RNA Sequencing reveals Injury induced Renal Developmental program reactivation and Lineage Infidelity in adult kidney

Project description:Acute Kidney Injury (AKI) is a rapid renal function decline associated with pronounced morbidity and mortality. Single Cell RNA Sequencing is a powerful tool allowing for examining transcriptional changes in multiple renal cell populations involved in the injury response. Our study reveals renal developmental gene re-activation and lineage infidelity in response to ischemia/reperfusion induced AKI, along with the novel genes which might serve as markers of acute kidney disease

2020-10-30 | GSE139506 | GEO

Reduced Abd-B Hox function during kidney development results in lineage infidelity

Project description:In this study, in order to better understand shared core Hox functions, we examined kidney development in mice with frameshift mutations of multiple Abd-B type Hox genes. The resulting phenotypes included dramatically reduced branching morphogenesis of the uretreric bud, premature depletion of nephron progenitors and abnormal development of the stromal compartment. Most unexpected, however, we also observed a cellular level lineage infidelity in nephron segments.

2018-01-20 | GSE109404 | GEO

Renal congestion exacerbates acute kidney injury in mice

Project description:The number of heart failure (HF) patients is increasing. HF is frequently accompanied by kidney dysfunction and such organ failure is closely related. Recent investigations revealed that increased renal venous pressure, rather than decreased cardiac output, causes the deterioration of kidney function in HF patients; however, the underlying responsible mechanisms are unknown. We demonstrated that reduced blood flow speed in peritubular capillaries (PTCs) by renal congestion and upregulation of nuclear factor-κB (NF-κB) signaling synergistically exacerbate kidney injury. We generated a novel mouse model with unilateral renal congestion by coarctation of the inferior vena cava between renal veins. Intravital imaging highlighted the notable dilatation of PTCs and decreased renal blood flow speed in the congestive kidney. Renal damage after ischemia reperfusion injury was exacerbated in the congestive kidney and accumulation of polymorphonuclear leukocytes (PMNs) within PTCs was observed at the acute phase after injury. Pharmacological inhibition of NF-κB ameliorated renal congestion-mediated exacerbation of kidney injury. In vitro, adhesion of PMNs on the TNFα-stimulated endothelial cells was accelerated by perfusion of PMNs at a slower speed, which was cancelled by the inhibition of NF-κB signaling. Our study demonstrates the importance of slower blood flow accompanying activated NF-κB signaling in the congestive kidney in the exacerbation of renal injury. These mechanisms may explain how increased renal venous pressure in HF patients causes the deterioration of kidney dysfunction. Inhibition of NF-κB signaling may be a therapeutic candidate for the vicious cycle between heart and kidney failure with increased renal venous pressure.

2024-02-16 | GSE166838 | GEO

Propofol and Sevoflurane Anesthesia in Colorectal Cancer Surgery: Incidence of Acute Kidney Injury

Project description:The goal of this observational study is to compare anesthetic modalities (intravenous propofol anesthesia with sevoflurane gas anesthesia) in patients who underwent colorectal cancer resection surgery regarding the outcome of acute kidney injury. The main questions it aims to answer are: * is there a difference in acute kidney injury incidence in the two anesthetic modalities? * is there a difference in plasma creatinine between the two anesthetic modalities? * are there any patient characteristics or intraoperative factors that effect the incidence of acute kidney injury in either anesthetic modality? The study will analyze data from the CAN clinical trial database. (Cancer and Anesthesia: Survival After Radical Surgery - a Comparison Between Propofol or Sevoflurane Anesthesia, NCT01975064)

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Glutamine attenuates renal ischemia-reperfusion injury and prevents acute kidney damage

Project description:Acute kidney injury (AKI) represents a common complication in critically ill patients that is associated with an increased morbidity and mortality. Currently, no effective treatment options are available. Here, we show that glutamine significantly attenuates leukocyte recruitment and inflammatory signaling in human and murine tubular epithelial cells (TECs). In a murine AKI model induced by ischemia-reperfusion-injury (IRI) we show that glutamine causes transcriptomic and proteomic reprogramming in renal TECs and neutrophils, resulting in decreased epithelial apoptosis, neutrophil recruitment and improved mitochondrial functionality and respiration provoked by an ameliorated oxidative phosphorylation. We identify the proteins glutamine gamma glutamyltransferase 2 (Tgm2) and apoptosis signal-regulating kinase (Ask1) as the major targets of glutamine in apoptotic signaling. Increased Tgm2 expression and reduced Ask1 activation result in decreased JNK activation leading to a diminished mitochondrial intrinsic apoptosis in kidneys upon IRI-induced AKI and under hypoxia or following TNFα-treatment of TECs. Consequently, glutamine administration attenuated kidney injury in vivo during AKI progression as well as TEC viability in vitro under inflammatory and hypoxic conditions.

2023-03-11 | PXD029723 | Pride

Renal congestion exacerbates acute kidney injury in mice

Project description:Renal congestion exacerbates acute kidney injury in mice

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Kidney gene expression profile following the transplant-induced reactivation of MCMV

Project description:Reactivation of latent HCMV is a significant infectious complication of organ transplantation, and current therapies target viral replication once reactivation of transcriptionally silent, latent virus has already occurred. The specific molecular pathways that activate viral gene expression are not well understood. Our studies aim to identify these factors, with the goal of developing novel therapies that prevent transcriptional reactivation in transplant recipients. MCMV is a valuable model for studying latency and reactivation of CMV induced by organ transplantation. We previously demonstrated that transplantation of MCMV-latently infected kidneys into allogeneic recipients induces transcriptional reactivation of immediate early (IE) gene expression within 48 hr. We used microarrays to profile global mouse kidney gene expression associated with transcriptional reactivation of MCMV immediate early gene expression at 48 hr after transplant of MCMV latently infected kidneys into allogeneic recipients. We identified differentially expressed genes and pathways associated with both early acute rejection and reactivation of MCMV. control vs. allograft

2015-08-27 | E-GEOD-72392 | biostudies-arrayexpress

Glutamine attenuates renal ischemia-reperfusion injury and prevents acute kidney damage

Project description:Our study investigates how the systemic administration of glutamine modulates the transcriptomic profile of neutrophils and renal tubular epithelial cells in the kidney during acute kidney injury.

2021-11-13 | GSE188628 | GEO

Implant renal injury-responsive cells to supplement erythropoietin and protect kidney [Spatial Transcriptomics]

Project description:Anemia poses a life-threatening risk to individuals with chronic kidney diseases (CKDs). Insufficient production of erythropoietin (EPO) from injured kidney is the major reason for anemia, while lack of EPO would further aggravate the kidney injury and make a “vicious cycle”. In this study, we dissected the change of endogenous EPO signaling in injured kidney by spatial transcriptomic analysis and validated the dual beneficial effects of local recombinant EPO administration on both anemia correction and kidney protection. Next, we constructed an injury-responsive EPO producing (iREP) element to sense the kidney damage signal and drive the synthesis and secretion of native EPO. After intra-renal implantation of iREP engineered HEK-293T embryonic kidney cells, the mouse kidney would automatically produce more EPO when sensing injury signal, which in turn enhanced red blood cell mass and protected kidney from further injury. Moreover, aided with automated equipment, we cloned urine-derived SOX9+ epithelial cells (USCs) from both healthy donors or CKD patients. The USCs could be transplanted into mouse kidney and form tubule-like structures, which makes them an alternative candidate cell for iREP engineering. Altogether, the current work proposed a potential approach based on engineered “smart” cell to treat CKDs.

2025-06-01 | GSE268847 | GEO

Plasminogen activator inhibitor-2 regulates immune response in kidney injury and renal aging mpact of plasminogen activator inhibitor-2 in kidney injury and renal aging

Project description:The plasminogen activator inhibitor-2 (PAI-2; encoded by the SerpinB2 gene) has been described in the context of macrophage activation and in cellular senescence. As both mechanisms are important in kidney disease we tested a possible role of PAI-2 in renal injury and repair. Methods:Aging, ischemia/reperfusion injury and unilateral ureteral obstruction were performed on the mice. Bone marrow was transplantefrom SerpinB2-/- to wild-type littermates and vice versa. Primary tubular cells and macrophages from SerpinB2-/- and wildtype mice were used for functional studies and transcriptional profiling. Results: PAI-2 expression was up-regulated in cultured senescent tubular cells and in kidneys of aged mice. In the lack of PAI-2 in SerpinB2-/- mice was associated with enhanced renal fibrosis and an inflammatory phenotype during aging and in kidney injury models. While acute injury was associated with fewer monocytes/macrophages in SerpinB2-/- kidneys the subsequent resolution of inflammation seen in wildtype kidneys was lacking in knockout mice. Conclusion: PAI-2 regulates renal aging, tubular damage, and resolution of inflammation. PAI-2 is crucial for kidney repair in mice .

2019-10-22 | GSE139156 | GEO

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