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Cross-species transcriptional network analysis defines shared inflammatory responses in murine and human lupus nephritis [Glomeruli]

ABSTRACT: 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

ORGANISM(S): Homo sapiens

PROVIDER: GSE37460 | GEO | 2012/12/10

SECONDARY ACCESSION(S): PRJNA160205

REPOSITORIES: GEO

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Cross-species transcriptional network analysis defines shared inflammatory responses in murine and human lupus nephritis [Glomeruli]

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

Cross-species transcriptional network analysis defines shared inflammatory responses in murine and human lupus nephritis[Tubulointerstitial]

Project description:Expression data from human with hypertensive nephropathy (HT) We used microarrays to analyze the transcriptome of microdissected renal biopsies from patients with HT

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Cross-species transcriptional network analysis defines shared inflammatory responses in murine and human lupus nephritis[Tubulointerstitial]

Project description:Expression data from human with hypertensive nephropathy (HT) We used microarrays to analyze the transcriptome of microdissected renal biopsies from patients with HT RNA from glomeruli and tubulointerstitial compartments was extracted and processed for hybridization on Affymetrix microarrays.

2012-12-10 | E-GEOD-37455 | biostudies-arrayexpress

RNA-seq for hand-microdissected glomeruli from Immunoglobulin A nephropathy patients

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Expression data from human with IgA nephropathy (IgAN)

Project description:This SuperSeries is composed of the following subset Series: GSE35487: Expression data from human with IgA nephropathy (IgAN) [HG-U133A] GSE35488: Expression data from human with IgA nephropathy (IgAN) [HG-U133A_ENTREZG_10] Refer to individual Series

2012-02-02 | E-GEOD-35489 | biostudies-arrayexpress

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Project description:The present study aimed to clarify the potential diagnosis value of the urinary N-glycoproteins using mass spectrometry (MS) analysis in patients with IgA nephropathy (IgAN).

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Project description:The current study makes use of NanoString targeted technology to profile urinary exosomal miRNAs from IgA nephropathy affected patients and corresponding healthy controls. Circulatory biomarkers were detected for IgA nephropathy from Indian cohort which can be made used for the diagnostic therapy. 14 miRNAs were detected to be related to the disregulation in miRNome of IgA nephropathy patients using lasso feature selection method, out of which multiple miRNAs like hsa.mir.146b.3p, hsa.mir.599 and many more was resulted with high AUROC values >=0.9 efficient in differentiating between healthy controls and IgA nephropathy condition. These markers can be use further in the diagnosis and treatment of IgAN.

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MicroRNA-21-5p participate in IgA nephropathy by driving T helper cell polarization

Project description:Previous studies revealed the abnormal lymphocytes subsets in IgA nephropathy (IgAN). Recently, emerging studies indicate that microRNA could influence the balance of T helper differentiation and function. Here we explore the underlying mechanism regarding how miRNA regulated lymphocytes subsets in IgAN, focused on T helper cell polarization.

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MicroRNA-21-5p participate in IgA nephropathy by driving T helper cell polarization [array]

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Project description:IgA nephropathy (IgAN), the most common primary glomerulonephritis worldwide, is characterized by IgA1-containing glomerular immunodeposits. These immunodeposits are thought to originate from the circulating immune complexes consisting of aberrantly glycosylated IgA1 (galactose-deficient IgA1; Gd-IgA1) bound by IgG autoantibodies. This hypothesis is supported by the findings that renal immunodeposits of IgA nephropathy patients are enriched for IgG autoantibodies specific for galactose-deficient IgA1 (Rizk et al., J. Am. Soc. Nephrol. 30(10), 2017-2026, 2019). However, experimental proof is needed. This study provides in vivo data in mice that support the pathogenic role of IgG autoantibodies in IgAN.

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