Aristolochic Acid Nephropathy 2 week time point of CD45+ cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE228516 | GEO | 2024/03/31
REPOSITORIES: GEO
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Project description:Aristolochic acid (AA) is a nephrotoxic carcinogen responsible for acute kidney injury, chronic renal failure, and associated urothelial cancers. This study aims to determine the genes in xenobiotic metabolism pathway regulated by AA and clarify the molecular mechanism underlying their action.
2018-05-09 | GSE101530 | GEO
Project description:Background Chronic kidney disease (CKD) is the progressive loss of renal function. Although advances have been made in understanding the progression of CKD, key molecular events in complex pathophysiological mechanisms that mark each stage of renal failure remain largely unknown. Changes in plasma protein profiles in different disease stages are important for identification of early diagnostic markers and potential therapeutic targets. The goal of this study was to determine the molecular profile of each CKD stage (from 1 to 5), aiming to specifically point out markedly expressed or downregulated proteins. Methods We performed a cross-sectional shotgun-proteomic study of plasma proteome across CKD stages and compared them to healthy controls. After sample pooling and heparin-column purification we analysed proteomes from healthy to CKD stage 1 through 5 participants’ plasma by liquid-chromatography/mass-spectrometry. Results We identified 298 proteins in all study groups, as well as several outliers. Our results indicate that key events, that may later affect the course of disease progression and the overall pathophysiological background, are most pronounced in CKD stage 2, with an emphasis on inflammation, lipoprotein metabolism, angiogenesis and tissue regeneration. Conclusions Our data is consistent with multiple previous studies in CKD research, but also uncovers previously unknown CKD mediators and brings forth several novel potential protein-candidates which might have a significant impact on the development of diagnostic and therapeutic strategies for CKD. We hypothesize that CKD stage 2 is the tipping point in disease progression and a suitable point in disease course for the development of therapeutic solutions.
2022-08-12 | PXD033427 | Pride
Project description:Chronic kidney disease (CKD) remains a tremendous and growing burden on the healthcare system and new therapies are needed to prevent or slow disease progression. Metabolic dysregulation and mitochondrial dysfunction are important features of acute and chronic tissue injury across species, and human genetics and preclinical data suggest that the master metabolic regulator 5'-adenosine monophosphate activated protein kinase (AMPK) may be an effective therapeutic target for CKD. Merck has recently disclosed a pan-AMPK activator MK-8722 which was shown to have beneficial effects on metabolic parameters in preclinical models. In this study we investigate the effects of MK-8722 in a progressive model of diabetic nephropathy to determine whether activation of AMPK would be of therapeutic benefit. We find that MK-8722 administration in a therapeutic paradigm is profoundly reno-protective. We provide evidence that the therapeutic effects may be mediated by modulation of renal mitochondrial quality control as well as by attenuating fibrotic and lipotoxic mechanisms in kidney cells. These data further validate the concept that targeting metabolic dysregulation in CKD could be a potential therapeutic approach.
2019-07-25 | GSE134804 | GEO
Project description:Intestinal epithelial cells (IEC) express large amounts of major histocompatibility complex II (MHCII) molecules. Despite this long-appreciated observation, the function of epithelial MHCII-mediated signaling on gut homeostasis remains enigmatic. As IECs serve as the primary cellular barrier between intestinal microbes and underlying host immune cells, we reasoned that IEC-intrinsic antigen presentation may play a role in tolerogenic responses towards the microbiota. Mice with an IEC-intrinsic defect in MHCII expression (IECΔMHCII) develop elevated T cell-dependent IgA responses, but a reduction in microbiota responsive regulatory T cells (Tregs). Despite elevated IgA levels in IECΔMHCII mice, immunoglobulin repertoires exhibit less selection and IgA has reduced reactivity to the microbiota, which is associated with increased inter-individual variability in microbiota composition. Consistent with reductions in microbiota-responsive Tregs, IECΔMHCII mice develop worsened colitis. A striking difference observed in the absence of IEC-MHCII is that while transcription of MHCII is similar, underlying mononuclear phagocytes had reduced surface MHCII. Macrophages were found to be capable of acquiring MHCII molecules from IECs, and macrophages isolated from IECΔMHCII mice had decreased capacity to stimulate Treg development. Thus, epithelial-myeloid interactions govern development of adaptive responses to microbial antigens within the gastrointestinal tract.
2021-09-09 | GSE183709 | GEO
Project description:Transcriptomes from hearts of control and CKD rats after transplantation of healthy kidney and kidney from CKD animal.
2019-10-01 | GSE88910 | GEO
Project description:Background – Acute kidney injury (AKI) is a devastating clinical condition affecting at least two-thirds of critically ill patients and among these patients is associated with a greater than 60% risk of mortality. Kidney mononuclear phagocytes (MP) are necessary for pathogenesis and healing in mouse models of AKI and thus have been the subject of investigation as potential targets for clinical interventions. Methods and Results – We have determined that, after injury, F4/80Hi-expressing kidney resident macrophages (KRM) are a distinct cellular subpopulation that does not differentiate from non-resident infiltrating MP. However, if KRM are depleted using polyinosinic:polycytidylic acid (poly I:C), they can be reconstituted from bone marrow derived precursors. Further, KRM lack major histocompatibility complex class II (MHCII) expression before post-parturition day 7 (P7) but upregulate it over the next 14 days. This MHCII- KRM phenotype reappears after injury. RNA sequencing shows injury causes transcriptional reprogramming of KRM to more closely resemble that found at P7. Post-injury KRM are also enriched in Wingless-type MMTV integration site family (Wnt) signaling, indicating a pathway vital for mouse and human kidney development is active. Conclusions – These data indicate that mechanisms involved in kidney development may be active after injury in KRM.
2019-04-16 | GSE121410 | GEO
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Project description:Mineral and bone disorder (MBD) is observed universally in patients with chronic kidney disease (CKD). Detrimental MBD-related skeletal changes include increased prevalence of fracture, cardiovascular disease, and mortality. MicroRNAs (miRNAs) have been identified as useful biomarkers in various diseases, and the aim of this study was to identify miRNAs associated with parathyroid hormone level in peritoneal dialysis (PD) patients. The PD patients were enrolled and grouped by their intact parathyroid hormone (iPTH) levels. Of the patients, total RNA was extracted from whole blood samples (n=15) and underwent miRNA microarray analysis.
2016-12-08 | GSE90991 | GEO
Project description:We aimed to identify urinary exosomal ncRNAs as novel biomarkers for diagnosis of Chronic Kidney Disease (CKD) for this, we examined 15 exosomal ncRNA profiles in urine samples from CKD patients from four different stages (I, II, III and IV) and compared them to 10 healthy controls. We identified a significant number of novel, differentially expressed ncRNAs in CKD patients compared to healthy, which might be employed as early diagnostic markers in CKD in the future.
2016-11-30 | E-MTAB-5152 | biostudies-arrayexpress