Ontology highlight
ABSTRACT:
PROVIDER: PRJNA669346 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12831148_1.fastq.gz | Fastqsanger.gz | |||
| SRR12831148_2.fastq.gz | Fastqsanger.gz | |||
| SRR12831149_1.fastq.gz | Fastqsanger.gz | |||
| SRR12831149_2.fastq.gz | Fastqsanger.gz | |||
| SRR12831150_1.fastq.gz | Fastqsanger.gz |
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Project description:Expression data from human with IgA nephropathy (IgAN) and hypertensive nephropathy (HT) We used microarrays to analyze the transcriptome of microdissected renal biopsies from patients with IgAN and HT RNA from glomeruli and tubulointerstitial compartments was extracted and processed for hybridization on Affymetrix microarrays.
2012-12-10 | E-GEOD-37460 | biostudies-arrayexpress
Project description:We collected glomeruli from biopsy specimens from IgA nephropathy patients with relatively preserved kidney function (eGFR ≥ 60 mL/min/1.73 m2 and urine protein-to-creatinine ratio < 3 g/g) and from normal kidney cortices by hand microdissection and performed RNA-seq. The transcriptomic profiling of IgA nephropathy glomerulus provide insights for intraglomerular pathophysiology of IgAN before reaching profound kidney dysfunction.
2020-09-30 | GSE141295 | GEO
Project description:IgA nephropathy (IgAN) is an autoimmune disease that involves galactose-deficient IgA1 (Gal-deficient IgA1) recognized by autoantibodies to form circulating immune complexes (IgA1-IC). Some of these complexes deposit in the glomeruli and induce kidney injury. Gal-deficient IgA1 alone is not sufficient to induce kidney damage. Additional proteins are required to form nephritogenic complexes. In this study, we isolated different molecular forms of serum IgA1, including IgA1-IC, monomeric (mIgA1), and polymeric (pIgA1) by SEC from patients with IgAN and healthy control donors. These three chromatographic fractions of molecular forms of IgA1 were analyzed by LC-MS. An analysis of the proteomes of the IgA1 molecular forms yielded several serum proteins enriched in the IgA1-IC. These proteins were also enriched in patients with IgAN when compared to healthy controls. The ability to characterize the proteome of IgA1-IC provides critical information relevant to IgAN pathogenesis and the nephritogenic characteristics of the ICs.
2025-11-03 | PXD055562 | Pride
Project description:IgA nephropathy (IgAN) is a common form of glomerulonephritis, according to the established multi-hit theory of IgAN pathogenesis, the final hit is the mesangial deposition of IgA1-containing immune complexes, leading to characteristic pathological features such as mesangial cell proliferation and expansion of extracellular matrix. We analyzed several public transcriptomic datasets, including microarray and bulk RNA-sequencing, to identify pathway alterations in IgAN patients and progressors. We also generated our own single-nucleus RNA-sequencing dataset from IgAN kidney biopsies with normal or reduced estimated glomerular filtration rate and integrated it with a publicly available healthy control dataset to comprehensively examine cell type specific changes during IgAN progression. Pathways related to complement activation, focal adhesion, and collagen formation were significantly enhanced in IgAN compared to healthy controls. Our snRNA-seq data identified two mesenchymal stromal cell (MSC) clusters with higher scores in these pathways than other cell types, which were progressively perturbed as eGFR declined. We observed a potential transition from mesangial cells to myofibroblasts within MSCs, accompanied by increased expression of genes involved in complement activation, humoral immunity, collagen organization, and extracellular matrix assembly. This transition could be partially reversed through in silico knockdown of certain transcription factors, such as PRRX1.
2025-01-18 | GSE286911 | GEO
Project description:Immunoglobulin A Nephropathy (IgAN) is a complex multifactorial disease whose genetic bases remain unknown. Distinct linkage and genome-wide association studies in both familial and sporadic IgAN suggest that there is a strong genetic component in IgAN. In this context, an intriguing role could be ascribed to copy number variants (CNVs) that have been recognized as an important source of genetic variation in humans. Here, we performed a whole-genome screening of CNVs in IgAN patients, their healthy relatives and healthy subjects (HS). A total of 217 individuals consisting of 51 IgAN cases and 166 healthy relatives were included in the initial screening. The high-throughput analysis of structural genetic variations, to find concordant aberrations across classes of samples, identified 178 IgAN-specific aberrations, specifically 114 loss and 64 gain. Several CNVs overlapped with regions evidenced by previous genome-wide genetic studies. Moreover, we found that IgAN patients characterized by deteriorated renal function carried low copy numbers of a CNV in chromosome 3 (chr3_loss:52031010-52260722). This CNV contained the TLR9 gene whose expression significantly correlated with the loss aberration in patients with progressive renal damage. Conversely, IgAN patients with normal renal function had no chr3_loss:52031010-52260722 and the TLR9 mRNA was expressed at the same level as in HS, still maintaining a strong correlation with the CNV. In conclusion, here we performed the first genome-wide CNV study in IgAN identifying some structural variants specific to IgAN patients and providing a collection of new candidate genes and loci that could help to dissect the complex genomic setting of the disease. Moreover, we identified a specific CNV, spanning the TLR9 gene, which could explain the disease severity in IgAN patients.
2014-10-30 | GSE44974 | GEO
Project description:In order to understand the kidney compartment specific epigenetic feature of glomeruli, we isolated glomeruli from human kidney biopsy and performed H3K27ac ChIP seq.
2021-03-26 | GSE142593 | GEO
Project description:Immunoglobulin A nephropathy (IgAN) is the most common form of primary glomerulonephritis worldwide characterized by aberrant O-glycosylation in the hinge region of IgA1. The basis for the abnormal glycosylation in IgAN is still unknown, but an important involvement of the enzyme core 1, beta 1,3-galactosyltransferase 1 (C1GALT1) is known. However, the role of microRNAs (miRNAs), a new family of key mRNA regulatory molecules, in the IgAN pathogenesis has not yet been reported. In this study, by high-throughput microRNA profiling, we identified 37 miRNAs differentially expressed in peripheral blood mononuclear cells (PBMCs) from IgAN patients compared to healthy subjects. Among them, upregulated miR-148b potentially targeted C1GALT1, INVS and PTEN, three genes notably downregulated in IgAN patients. C1GALT1 expression levels in IgAN patients were reduced and negatively correlated with the upregulated miR-148b expression. We demonstrated the biological relationship between miR-148b and C1GALT1 by transient transfection experiments ex vivo. When we reduced the upregulated miR-148b function in PBMCs of IgAN patients an increase of the C1GALT1 mRNA and protein levels was observed. We validated biologically also the miR-148b targeting of INVS , involved in the altered modulation of the WNT–β-catenin and PI3K/Akt pathways in IgAN patients. All together our data evidence an important role of miR-148b in the pathogenesis of IgAN, which could explain the aberrant glycosylation of IgA1 in the pathogenesis and should light on a potential target for the theraphy of the disease.
2012-03-12 | GSE25590 | GEO
Project description:Purpose: Immunoglobulin A nephropathy (IgAN) is immune-mediated primary glomerulonephritis, which is the most common reason leading to renal failure worldwide, the exact pathogenesis of IgAN is not well defined. Accumulating evidence indicates that circular RNAs (circRNAs) play crucial roles in the immune disease by involving in the competing endogenous RNA (ceRNA) network mechanism. At present, the studies of the circRNA profiles and circRNA-associated ceRNA networks in the IgAN are still scarce. This study aimed to elucidate the potential roles of circRNA, microRNA (miRNA), and messenger RNA (mRNA) ceRNA network in peripheral blood mononuclear cells (PBMCs) of IgAN. Methods: CircRNA sequencing was used to identify the differential expressed circRNAs (DEcircRNAs) of PBMCs in IgAN and healthy controls. A circRNA-miRNA-mRNA ceRNA network was constructed to further investigate the mechanisms of IgAN. Results: A total of 145 circRNAs were differentially expressed in IgAN compared with controls (|log2 (FC)|>1 and P-value <0.05). Combined with the data from GSE73953 and GSE25590 in GEO database, a ceRNA network was constructed which contained 16 DEcircRNAs, 72 differential expressed mRNAs (DEmRNAs) and 11 differential expressed miRNAs (DEmiRNAs). Conclusion: Our study identified a novel circRNA-mediated ceRNA regulatory network mechanisms in the pathogenesis of IgAN.
2020-11-08 | GSE154046 | GEO
Project description:Immunoglobulin A nephropathy (IgAN) is the most common glomerulonephritis worldwide. However, biomarkers for predicting the progression or regression of IgAN remain a clinical challenge. In the present study, we aim to identify novel diagnostic and prognostic markers of IgAN. Using the cytokine antibody array, we detected serum and urinary levels of nine potential IgAN biomarkers in 32 IgAN patients and 16 healthy controls. The IgAN patients were grouped according to Lee’s grading system, with 16 patients with Grade I–II in the mild IgAN group and 16 with Grade III-V in the severe IgAN group. The associations between levels of these markers and IgAN were evaluated.
2022-07-13 | E-MTAB-11972 | biostudies-arrayexpress