Next generation sequencing of miRNAs in folic acid-induced kidney damage
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE61328 | GEO | 2015/12/22
SECONDARY ACCESSION(S): PRJNA260787
REPOSITORIES: GEO
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Project description:We have used small RNA sequencing to measure the expression of all miRNAs present in the kidneys during the development of folic acid-induced kidney injury and fibrosis. From this miRNA expression profile, we identified miRNAs associated with different stages and aspects of kidney damage. BALB/c mice were injected with 250mg/kg of folic acid and kidneys were collected at 0, 1, 2, 3, 7, 14, and 28 days. Total RNA was prepared for sequencing using the Illumina TruSeq Small RNA Sample Preparation Kit, and analyzed on an Illumina HiSeq 2000.
2015-12-22 | E-GEOD-61328 | biostudies-arrayexpress
Project description:Treatments for kidney fibrosis represent an urgent yet unmet clinical need. Effective therapies are limited due to not well understood molecular pathogenesis. We aimed at generating a comprehensive and integrated multi-omics data set (RNA/ microRNA transcriptomics and proteomics) of fibrotic kidneys which will be searchable through a user-friendly web application. Therefore, two commonly used mouse models were utilized: a reversible chemical-induced injury model (folic acid (FA) induced nephropathy) and an irreversible surgical-induced fibrosis model (unilateral ureteral obstruction (UUO)). RNA and small RNA sequencing as well as MS/MS with 10-plex tandem mass tags proteomics were performed with kidney samples from different time points over the course of fibrosis development. In summary, we present temporal and integrated multi-omics data from fibrotic mouse kidneys which are accessible through an interrogation tool to provide a searchable transcriptome and proteome for kidney fibrosis researcher.
2019-05-09 | PXD011453 | Pride
Project description:Treatments for kidney fibrosis represent an urgent yet unmet clinical need. Effective therapies are limited due to not well understood molecular pathogenesis. We aimed at generating a comprehensive and integrated multi-omics data set (RNA/ microRNA transcriptomics and proteomics) of fibrotic kidneys which will be searchable through a user-friendly web application. Therefore, two commonly used mouse models were utilized: a reversible chemical-induced injury model (folic acid (FA) induced nephropathy) and an irreversible surgical-induced fibrosis model (unilateral ureteral obstruction (UUO)). RNA and small RNA sequencing as well as MS/MS with 10-plex tandem mass tags proteomics were performed with kidney samples from different time points over the course of fibrosis development. In summary, we present temporal and integrated multi-omics data from fibrotic mouse kidneys which are accessible through an interrogation tool to provide a searchable transcriptome and proteome for kidney fibrosis researcher.
2019-05-09 | PXD010861 | Pride
Project description:Kidney fibrosis represents an urgent unmet clinical need due to the lack of effective therapies and inadequate understanding of the molecular pathogenesis. We have generated a comprehensive and integrated multi-omics data set (proteomics, mRNA and small RNA transcriptomics) of fibrotic kidneys that is searchable through a user-friendly web application. Two commonly used mouse models were utilized: a reversible chemical-induced injury model (folic acid (FA) induced nephropathy) and an irreversible surgically-induced fibrosis model (unilateral ureteral obstruction (UUO)). mRNA and small RNA sequencing as well as 10-plex tandem mass tag (TMT) proteomics were performed with kidney samples from different time points over the course of fibrosis development. The bioinformatics workflow used to process, technically validate, and integrate the single data sets will be described. In summary, we present temporal and integrated multi-omics data from fibrotic mouse kidneys that are accessible through an interrogation tool to provide a searchable transcriptome and proteome for kidney fibrosis researchers.
2019-05-07 | GSE126181 | GEO
Project description:Microarray analysis of human kidneys with acute kidney injury (AKI) has been limited because such kidneys are seldom biopsied. However, all kidney transplants experience AKI, and early kidney transplants without rejection are an excellent model for human AKI: they are screened to exclude chronic kidney disease, frequently biopsied, and have extensive follow-up. We used histopathology and microarrays to compare indication biopsies from 28 transplants with AKI to 11 pristine protocol biopsies of stable transplants. Kidneys with AKI showed increased expression of 394 injury-repair response associated transcripts, including many known epithelial injury molecules (e.g. ITGB6, LCN2), tissue remodeling molecules (e.g. VCAN), and inflammation molecules (S100A8, ITGB3). Many other genes also predict the phenotype, depending on statistical filtering rules, including AKI biomarkers as HAVCR1 and IL18. Most mouse orthologs of the top injury-repair transcripts were increased in published mouse AKI models. Pathway analysis of the injury-repair transcripts revealed similarities to cancer, development, and cell movement. The injury-repair transcript score AKI kidneys correlated with reduced function, future recovery, brain death, and need for dialysis, but not future graft loss. In contrast, histologic features of "acute tubular injury" did not correlate with function or with the molecular changes. Thus the injury-repair associated transcripts represent a massive coordinate injury-repair response of kidney parenchyma to AKI, similar to mouse AKI models, and provide an objective measure for assessing the severity of AKI in kidney biopsies and validation for the use of many AKI biomarkers.
2012-02-21 | GSE30718 | GEO
Project description:Gene expression profiles of Tert+/+ and generation 3 (G3) Tert-/- male an female mice were untretaed or tretaed witth Folic acid.
2021-01-21 | GSE162446 | GEO
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 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, AOAH expression was examined in human and mouse kidneys, and Aoah-/- mice and single cell RNA sequencing (scRNA-seq) were performed to determine its role in kidney injury induced by folic acid (FA). We found that AOAH expression was positively correlated with estimated glomerular filtration rate (eGFR) while negatively correlated with the degree of renal fibrosis in kidneys of CKD patients. AOAH deletion led to exacerbated kidney injury and fibrosis after FA administration, which was reversed by overexpression of Aoah in kidneys. scRNA-seq revealed that Aoah-/- mice exhibited increased subpopulation of CD74+ PTECs, even though total PTECs were decreased compared to WT mice after FA treatment. Finally, exacerbated kidney injury and fibrosis seen in Aoah-/- mice was attenuated via administration of ISO-1, an inhibitor of macrophage inhibition factor (MIF) and CD74 binding. 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
Project description:Acute kidney failure and chronic kidney disease are global health issues steadily rising in incidence and prevalence. Animal models are critically needed to better understand these diseases and develop new therapies. These models are typically restricted to a single genetic background, thus fail to recapitulate the hallmarks of human nephropathies and the diversity of their associated clinical presentations. Here, we used a simple model of folic acid-induced kidney injury in 7 highly diverse mouse strains. We measure plasma and urine parameters, as well as renal histopathology and mRNA expression data at 1-, 2- and 6-weeks after folic acid administration, covering the early response and subsequent recovery from injury. We observe an extensive strain-specific response ranging from complete resistance of the CAST/EiJ to high sensitivity of the C57BL/6J, DBA/2J, and PWK/PhJ strains. We show that in these susceptible strains, the severe early kidney injury is accompanied by the induction of mitochondrial stress genes, which is associated with delayed healing and a prolonged inflammatory and adaptive immune responses 6 weeks after the insult, heralding a transition to chronic kidney disease. Our data catalogue the variability in predisposition to acute kidney injury, recovery, and transition to chronic kidney disease in laboratory strains, enabling better selection of mouse strains to study kidney disease.
2023-01-11 | GSE222570 | GEO
Project description:Short telomeres trigger epithelial to mesenchymal transition programmes and sensitize to folic acid-induced kidney fibrosis in mice [folic acid]
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Project description:Caco-2, HT29, CCD841CoTr exposed to 10ng/mL, 100ng/mL and 4000ng/mL folic acid
2010-06-10 | E-GEOD-2047 | biostudies-arrayexpress