Mus musculus
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ABSTRACT:
PROVIDER: PRJNA751142 | ENA |
REPOSITORIES: ENA
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Project description:microRNAs profiles of contrast-induced acute kidney injury rats
| PRJNA321466 | ENA
Project description:Sepsis-induced acute kidney injury (AKI) is the most common form of AKI with poor outcomes. Renal proteomic analysis after bacterial lipopolysaccharide (LPS) administration revealed that the local renal acute phase reaction (APR) is one of the strongest responses of the kidney during septic AKI in mice. Evaluation of mRNA expression confirmed that most acute phase proteins were produced in the kidney. Our study also provides missing information on the time course of septic renal APR. Proteomic analysis of LPS-induced AKI demonstrated a marked upregulation of local renal acute phase response (APR) that commenced a few hours post injection and peaked at 24 h. Much more APPs were involved in the renal APR than previously identified.
2020-01-08 | PXD014664 | Pride
Project description:characterization of fibrinogen expression in the kidney, excretion in the urine following kidney damage and evaluating the therapeutic potential of fibrinogen in acute kidney injury. Total RNA was isolated of renal cortex and medulla from rats subjected to 20 min of bilateral ischemia followed by 6, 24 120, hr of reperfusion compared to sham rats.
2011-09-30 | E-GEOD-27274 | biostudies-arrayexpress
Project description:In this study, we aimed to evaluate the effect of M2-like macrophages in the injured kidney on kidney cancer progression. As an acute kidney injury to chronic kidney disease model, we used unilateral ischemia-reperfusion injury (uIRI). And we inoculated RenCa cells, which are murine kidney cancer cell line, into renal subcapsule 14 days after uIRI (uIRI-Can) and compared uIRI-Can to RenCa cells inoculated into sham-operated renal subcapsule (Sham-Can) 20 days after inoculation. To identify gene characteristics of M2-like macrophages that are commonly detected both in the uIRI kidney cortex and uIRI-Can, we sorted Ly6Clow macrophages from 4 groups, uIRI kidney cortex, sham kidney cortex, uIRI-Can, and Sham-Can, and conducted RNA-Seq. This study revealed the characteristic gene expression of M2-like macrophages which were commonly detected in the injured kidney cortex and kidney cancer progressed on the injured kidney. And this could be a future therapeutic target of macrophage-targeted therapy.
2022-12-06 | GSE197494 | GEO
Project description:Although diabetic nephropathy (DN) is the most common cause for end-stage renal disease (ESRD) in western societies, its pathogenesis still remains largely unclear. A different gene pattern of diabetic and healthy kidney cells is one of the probable explanations. Numerous signaling pathways have emerged as important pathophysiological mechanisms for diabetes-induced renal injury. Glomerular cells, as podocytes or mesangial cells, are predominantly involved in the development of diabetic renal lesions. While a lot of gene assays concerning DN are performed with whole kidney or renal cortex tissue, we isolated glomeruli from BTBR ob/ob and wildtype mice at 4 different timepoints (4, 8, 16, 24 weeks) and performed a mRNA microarray to identify differentially expressed genes (DEGs). In contrast to many other diabetic mouse models, these homozygous ob/ob leptin-deficient mice do not only develop a severe type II diabetes, but also diabetic kidney injury with all the clinical and especially histologic features defining human DN. The identified DEGs in diabetic glomeruli were used to investigate biological processes and pathways enriched at different disease stages.
2017-12-10 | GSE106841 | GEO
Project description:Congenital obstructive nephropathy is a common cause of chronic kidney disease and a leading indication for renal transplant in children. The cellular and molecular responses of the kidney to congenital obstruction are incompletely characterized. In this study, we evaluated global transcription in kidneys with graded hydronephrosis in the megabladder (mgb-/-) mouse to better understand the pathophysiology of congenital obstructive nephropathy. Three primary pathways associated with kidney remodeling/repair were induced in mgb-/- kidneys independent of the degree of hydronephrosis. These pathways included retinoid signaling, steroid hormone metabolism, and renal response to injury. Urothelial proliferation and the expression of genes with roles in the integrity and maintenance of the renal urothelium were selectively increased in mgb-/- kidneys. Ngal/Lcn2, a marker of acute kidney injury, was elevated in 36% of kidneys with higher grades of hydronephrosis. Evaluation of Ngalhigh versus Ngallow kidneys identified the expression of several novel candidate markers of renal injury. This study indicates that the development of progressive hydronephrosis in mgb-/- mice results in renal adaptation that includes significant changes in the morphology and potential functionality of the renal urothelium. These observations will permit the development of novel biomarkers and therapeutic approaches to progressive renal injury in the context of congenital obstruction. Gene expression was measured in control, mild, moderate and severely hydronephrotic megabladder mouse kidneys. A total of 6 control kidneys were compared to 18 mutant kidneys from age-matched male animals.
2013-06-18 | E-GEOD-48041 | biostudies-arrayexpress
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
Project description:Ferroptosis is an iron-dependent programmed cell death associated with severe kidney diseases, linked to decreased glutathione peroxidase 4 (GPX4). However, the spatial distribution of renal GPX4-mediated ferroptosis and the molecular events causing GPX4 reduction during ischemia-reperfusion (I/R) remain largely unknown. Using spatial transcriptomics, we identify that GPX4 is situated at the interface of the inner cortex and outer medulla, a hyperactive ferroptosis site post-I/R injury. We show that OTU deubiquitinase 5 (OTUD5) is a GPX4-binding protein that confers ferroptosis resistance by stabilizing GPX4. During I/R, ferroptosis is induced by mTORC1-mediated autophagy, causing OTUD5 degradation and subsequent GPX4 decay. Functionally, OTUD5 deletion intensifies renal tubular cell ferroptosis and exacerbates acute kidney injury, while AAV-mediated OTUD5 delivery mitigates ferroptosis and promotes renal function recovery from I/R injury. In this work, our study highlights a new autophagy-dependent ferroptosis module: hypoxia/ischemia-induced OTUD5 autophagy triggers GPX4 degradation, offering a potential therapeutic avenue for I/R-related kidney diseases.
2023-11-29 | GSE244330 | GEO
Project description:Congenital obstructive nephropathy is a common cause of chronic kidney disease and a leading indication for renal transplant in children. The cellular and molecular responses of the kidney to congenital obstruction are incompletely characterized. In this study, we evaluated global transcription in kidneys with graded hydronephrosis in the megabladder (mgb-/-) mouse to better understand the pathophysiology of congenital obstructive nephropathy. Three primary pathways associated with kidney remodeling/repair were induced in mgb-/- kidneys independent of the degree of hydronephrosis. These pathways included retinoid signaling, steroid hormone metabolism, and renal response to injury. Urothelial proliferation and the expression of genes with roles in the integrity and maintenance of the renal urothelium were selectively increased in mgb-/- kidneys. Ngal/Lcn2, a marker of acute kidney injury, was elevated in 36% of kidneys with higher grades of hydronephrosis. Evaluation of Ngalhigh versus Ngallow kidneys identified the expression of several novel candidate markers of renal injury. This study indicates that the development of progressive hydronephrosis in mgb-/- mice results in renal adaptation that includes significant changes in the morphology and potential functionality of the renal urothelium. These observations will permit the development of novel biomarkers and therapeutic approaches to progressive renal injury in the context of congenital obstruction.
2013-06-18 | GSE48041 | GEO
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.
2012-08-15 | GSE34351 | GEO