MicroRNA in chronic kidney disease (CKD)
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE80247 | GEO | 2017/01/01
SECONDARY ACCESSION(S): PRJNA318387
REPOSITORIES: GEO
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Project description:Genetic Study of CHronic Kidney DIsease (CKD)
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Project description:Genetic Study of CHronic Kidney DIsease (CKD)
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Project description:Epidemiological studies indicate that adverse intrauterine and postnatal environment has a long-lasting role in chronic kidney disease (CKD) development. Epigenetic information can represent a plausible carrier for mediating this "programming" effect. Here we demonstrate that genome-wide cytosine methylation patterns of healthy and CKD tubule samples obtained from patients show significant differences. We rarely observed differentially methylated regions (DMR) on promoters. Histone modification-based kidney specific genome-wide gene regulatory region annotation maps (promoters, enhancers, transcribed and repressed regions) were generated. DMRs mostly overlapped with putative enhancer regions and were enriched in consensus binding sequences for important renal transcription factors, indicating their importance in gene expression regulation. A core set of genes, including transforming growth factors and collagens, showed cytosine methylation changes correlating with downstream transcript levels. Our report raises the possibility that epigenetic dysregulation plays a role in CKD development via influencing core profibrotic pathways. HG18_HELP array We used custom-commercial array to detail the differences of methylation regions of human tubule epithelial cells between chronic kidney disease and normal. We sought to decrease the cell type heterogeneity of kidney tissues to increase the resolution of methylation profiles. To that end, microdissected human kidney tissue from both chronic kidney disease patient and normal are used for the HELP-assay (HpaII tiny fragment Enrichment by Ligation-mediated PCR) and hybridization on Roche NimbleGen microarrays.
2013-08-09 | E-GEOD-49557 | biostudies-arrayexpress
Project description:Uremic cardiomyopathy is a clinically highly relevant cause of cardiovascular events in patients with chronic kidney disease (CKD). This study aimed at a comprehensive analysis of cardiac function and cardiac pathological characteristics in adenine-induced CKD in 129/Sv mice. This included the analysis of kidney function and morphology, heart function as well as cardiac hypertrophy, fibrosis and calcification. Also, cardiac RNA-sequencing was performed. Although overall, no cardiac dysfunction, hypertrophy or fibrosis could be observed, prolonged moderate CKD in this mouse model enhanced cardiac oxidative stress markers. In line, cardiac RNA-sequencing revealed an increase in oxidative stress-inducing signaling in CKD as well as anti-inflammatory feedback responses. This suggests a maladaptive preconditioning of the heart in CKD, which could increase the risk of enhanced cardiovascular damage upon additional cardiovascular risk factors and/or events.
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Project description:Epidemiological studies indicate that adverse intrauterine and postnatal environment has a long-lasting role in chronic kidney disease (CKD) development. Epigenetic information can represent a plausible carrier for mediating this programming effect. Here we demonstrate that genome-wide cytosine methylation patterns of healthy and CKD tubule samples obtained from patients show significant differences. Cytosine methylation changes showed high concordance (98%) with a large (n=87) replication dataset. We rarely observed differentially methylated regions (DMR) on promoters. Histone modification-based kidney specific genome-wide gene regulatory region annotation maps (promoters, enhancers, transcribed and repressed regions) were generated. DMRs mostly overlapped with putative enhancer regions and were enriched in consensus binding sequences for important renal transcription factors, indicating their importance in gene expression regulation. A core set of genes, including transforming growth factors and collagens, showed cytosine methylation changes correlating with downstream transcript levels. Our report raises the possibility that epigenetic dysregulation plays a role in CKD development via influencing core profibrotic pathways. We used microarrays to detail the differences of gene expression of human tubule epithelial cells between chronic kidney disease and normal. We sought to decrease the cell type heterogeneity of kidney tissues to increase the resolution of expression profiles. To that end, microdissected human kidney tissue from both chronic kidney disease patient and normal are used for RNA extraction and hybridization on Affymetrix microarrays.
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Project description:MicroRNAs (miRs) have the potential to be employed as diagnostic and prognostic biomarkers of chronic kidney disease (CKD) and are functionally important in disease pathogenesis. To identify novel miR biomarkers we performed small RNA-sequencing (sRNA-Seq) to detect miRs that were quantitatively altered in the circulation of individuals with type 2 diabetes (T2D) with CKD compared to those with normal kidney function. MiR-190a-5p abundance was significantly lower in the circulation of T2D patients with reduced kidney function compared to those with normal kidney function. To validate if the loss of circulating miR-190a-5p was associated with reduced kidney function we measured miR-190a-5p in an unselected cohort of CKD patients and determined if dysregulated miR-190a-5p could predict kidney outcomes. In individuals with no or moderate albuminuria (<300mg/mmol), serum miR-190a-5p levels predicted CKD progression (reaching end-stage kidney disease or >30% reduction from baseline eGFR, independent of age, sex, baseline eGFR, urinary albumin excretion, or blood pressure (adjusted HR 0.80, 95% CI: 0.66-0.96, p=0.015). To identify the kidney source of miR-190a-5p we utilised transcriptomic data from mouse models of kidney injury and single nuclear (sn) RNA-Seq from human kidney, finding that miR-190a-5p is enriched in the proximal tubule (PT) but down-regulated following injury. Bioinformatic analysis highlighted ADAM10as a potential miR-190a-5p target and we validated this in human PT cell line. Our analyses suggest that miR-190a-5p is a biomarker of tubular cell health and low circulating levels may predict CKD progression in patients with low or moderate proteinuria independent of existing risk factors.
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Project description:Systemic iron metabolism is disrupted in chronic kidney disease (CKD). However, little is known about local kidney iron homeostasis and its role in kidney fibrosis. Kidney-specific effects of iron therapy in CKD also remain elusive. Here, we elucidate the role of macrophage iron status in kidney fibrosis and demonstrate that it is a potential therapeutic target. In CKD, kidney macrophages exhibited depletion of labile iron pool (LIP) and induction of transferrin receptor 1, indicating intracellular iron deficiency. Low LIP in kidney macrophages was associated with their defective antioxidant response and proinflammatory polarization. Repletion of LIP in kidney macrophages through knockout of ferritin heavy chain (Fth1) reduced oxidative stress and mitigated fibrosis. Similar to Fth1 knockout, iron dextran therapy, through replenishing macrophage LIP, reduced oxidative stress, decreased the production of proinflammatory cytokines, and alleviated kidney fibrosis. Interestingly, iron markedly decreased TGF-β expression and suppressed TGF-β–driven fibrotic response of macrophages. Iron dextran therapy and FtH suppression had an additive protective effect against fibrosis. Adoptive transfer of iron-loaded macrophages alleviated kidney fibrosis, validating the protective effect of iron-replete macrophages in CKD. Thus, targeting intracellular iron deficiency of kidney macrophages in CKD can serve as a therapeutic opportunity to mitigate disease progression.
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