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Integrative peptidomics and proteomics profiling of plasma-derived extracellular vesicles reveals molecular signatures of SLE and LN

ABSTRACT: Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease for which non-invasive stratification of lupus nephritis (LN) remains challenging. Here, we integrated antibody-based enrichment of plasma-derived extracellular vesicles (EVs) with label-free peptidomic and proteomic profiling in a discovery cohort of 45 individuals comprising healthy controls, SLE without nephritis (SLE LN−), and SLE with nephritis (SLE LN+). A total of 472 endogenous peptides and 3,111 proteins were quantified. The EV proteome predominantly captured SLE-associated immune, complement-coagulation, and platelet signatures, whereas the endogenous peptidome exhibited greater discriminatory power for renal involvement. Compared with SLE LN− patients, SLE LN+ patients displayed 296 differentially expressed peptides, including 245 peptides specifically associated with LN-related comparisons. To verified the reproducibility and clinical relevance of EV molecular signatures, targeted multiple reaction monitoring (MRM) was perfor

ORGANISM(S): Homo Sapiens

SUBMITTER: Dong Wei

PROVIDER: PXD081843 | iProX | Tue Jul 28 00:00:00 BST 2026

REPOSITORIES: iProX

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Urinary Extracellular Vesicle Metabolomic Profiling Reveals a Distinct Molecular Signature for the Non-Invasive Diagnosis of Lupus Nephritis

Project description:Background: Lupus nephritis (LN) is a severe complication of systemic lupus erythematosus (SLE), underscoring an urgent need for non-invasive diagnostic biomarkers. Objective: This study aimed to define the metabolomic signature of urinary extracellular vesicles (uEVs) in LN and to identify novel biomarkers for precision diagnosis.Methods: We isolated uEVs from 29 patients with LN, 22 SLE patients without nephritis, and 20 healthy controls. uEVs were characterized according to MISEV guidelines, and their metabolomes were profiled using untargeted liquid chromatography–tandem mass spectrometry (LC–MS/MS). Differential metabolites were analyzed through bioinformatics and a random forest machine-learning algorithm to construct a diagnostic model. Results: Among 897 identified metabolites, 284 were significantly dysregulated in LN. A random forest model prioritized a ten-metabolite panel. Three metabolites—Glucosylsphingosine, PE-NMe, and PC(20:5/TXB2)—exhibited outstanding diagnostic performance, with area under the curve (AUC) values of 0.912, 0.906, and 0.897, respectively, for distinguishing LN from non-renal SLE. Conclusion: We identified a distinct uEV metabolic signature in LN and developed a robust, non-invasive biomarker panel. This strategy holds significant promise for the early detection and personalized management of LN, offering a compelling alternative to invasive renal biopsy.

2026-02-11 | MTBLS13839 | MetaboLights

Genetic Contributions of Lupus Nephritis in A Multi-Ethnic Cohort

Project description:Lupus nephritis (LN) is a severe manifestation of systemic lupus erythematosus (SLE) and it occurs at a much higher rate in patients that are not of European descent. The purpose of this study is to identify genetic variants contributing to the risk of LN in a multi-ethnic cohort of SLE patients. We used a comprehensive genome-wide screen and 1244 SLE patients from 5 different ethnic groups. In genome-wide gene-based and candidate SNP analyses, we found distinct genes and pathways, and established risk SNPs associated with lupus nephritis for each ethnic group. This study represents progress in elucidating the genetic underpinnings driving LN among SLE patients of different ethnic groups.

| phs001609 | dbGaP

Genome-wide peripheral blood transcriptome analysis of Arab female Lupus and Lupus nephritis

Project description:Genome-wide alternative splice analysis of RNA from lupus and its severe form lupus nephritis We aimed to explore the genome-wide peripheral blood transcriptome of lupus (SLE) and its severe form lupus nephritis (LN) cases compared to healthy subjects (HC) using high density Affymetrix Human Exon1.0.ST arrays. Analysis revealed 15 splice variants that are differentially expressed between SLE/HC and 99 variants between LN/HC (pâ¤0.05,SI>orâ¤0.5,Benjamin Hochberg-False discovery rate correction). Comparison between LN/SLE revealed 7 variants that are differentially expressed with pâ¤0.05,SI>0.5,Benjamin Hochberg-FDR correction. Pathway analysis of differentially spliced genes revealed 11 significant pathways in SLE and 12 in LN (p<0.05). Analysis of peripheral blood transcriptome revealed signature causative genes that are alternatively spliced, signifying their clinical relevance in the pathophysiology of disease. The extent of differential splicing was found to be higher in LN than in SLE, signifying the need for further in-depth research in the same domain. Present study is the first to reveal the significance of alternative variants in susceptibility to SLE and LN. We analyzed blood from 11 female subjects (5 lupus, 3 lupus nephritis and 3 healthy control) using the Affymetrix Human Exon 1.0 ST platform. Array data was processed by Alt Analyze and Genespring software. No techinical replicates were performed. One of the outiler sample (HC2) was excluded from further analysis.

2016-01-06 | E-GEOD-62764 | biostudies-arrayexpress

LncRNA expression profiling for 9 human plasma samples from systemic lupus erythematosus patients and healthy controls

Project description:To screen the differentially expressed lncRNAs, we performed lncRNA profiling using ArrayStar Human LncRNA Microarray in 24 new-onset systemic lupus erythematosus (SLE) patients and 12 age- and sex-matched healthy controls (HCs). For the lncRNA microarray screening, total RNA from plasma was isolated from 12 SLE without nephritis, 12 lupus nephritis (LN) and 12 HCs. Four RNA samples were mixed togther as a pool of sample for microarray analysis. Accordingly, there were each three pooled RNA samples from 12 SLE without nephritis, 12 LN and 12 HCs for microarray analysis. Hierarchical clustering showed the plasma levels of lncRNAs and mRNAs differed significantly between 24 new-onset SLE patients and 12 control subjects. With a fold change ≥ 2 and P ≤ 0.05, we identified 1315 significantly differentially expressed lncRNAs (743 lncRNAs up-regulated and 572 lncRNAs down-regulated) and 1363 differentially expressed mRNAs (745 mRNAs up-regulated and 618 mRNAs down-regulated) in plasma of SLE patients compared with control samples.

2017-08-12 | GSE102547 | GEO

Transcriptomic profiling of Aurora Kinase B inhibition in lupus-prone mice

Project description:Lupus nephritis (LN) is one of the most common and severe complications of systemic lupus erythematosus (SLE). Multitarget therapy (MT) has demonstrated a 20% higher rate of complete remission (CR) compared to conventional treatments for LN. Using a signature-based approach for drug repurposing, we identified and validated that the specific Aurora Kinase B (AURKB) inhibitor AZD1152 exhibits therapeutic efficacy comparable to that of MT therapy. To elucidate the therapeutic mechanism of AZD1152, we conducted transcriptome sequencing on renal tissues from MRL/lpr mice treated with AZD1152 and control vehicle. ,

2025-02-05 | GSE277837 | GEO

Genome-wide peripheral blood transcriptome analysis of Arab female Lupus and Lupus nephritis

Project description:Genome-wide alternative splice analysis of RNA from lupus and its severe form lupus nephritis We aimed to explore the genome-wide peripheral blood transcriptome of lupus (SLE) and its severe form lupus nephritis (LN) cases compared to healthy subjects (HC) using high density Affymetrix Human Exon1.0.ST arrays. Analysis revealed 15 splice variants that are differentially expressed between SLE/HC and 99 variants between LN/HC (p≤0.05,SI>or≤0.5,Benjamin Hochberg-False discovery rate correction). Comparison between LN/SLE revealed 7 variants that are differentially expressed with p≤0.05,SI>0.5,Benjamin Hochberg-FDR correction. Pathway analysis of differentially spliced genes revealed 11 significant pathways in SLE and 12 in LN (p<0.05). Analysis of peripheral blood transcriptome revealed signature causative genes that are alternatively spliced, signifying their clinical relevance in the pathophysiology of disease. The extent of differential splicing was found to be higher in LN than in SLE, signifying the need for further in-depth research in the same domain. Present study is the first to reveal the significance of alternative variants in susceptibility to SLE and LN.

2016-01-06 | GSE62764 | GEO

Lupus Nephritis is characterized by defective removal of Neutrophil Extracellular Traps that are modified in protein composition and contain specific auto-antigens.

Project description:Neutrophyl Extracellular Traps (NETs) accumulated in serum of patients with Lupus Nephritis for defective removal by DNAse. Among a complex protein panel (overall 802) two clusters of 16 and 13 proteins were more expressed by LN and SLE NETs respectively; oxidized aenolase and annexin A1 were main components of the first series in LN. NETs may represent a source of modified intracellular antigens for autoimmunity in LN.

2019-11-12 | PXD007754 | Pride

Next generation sequencing facilitates quantitative analysis of tissue-specific molecular signatures in lupus mice

Project description:Purpose: Next-generation sequencing (NGS) technology was used to map expression profiles of effector (spleen) and key target tissues (kidney and brain) in mouse model of Systemic Lupus Erythematosus (SLE). Methods: Total RNA was extracted from total brain, total kidney and total spleen using Trizol and mRNA libraries were generated using the Illumina TruSeq Sample Preparation kit v2. Paired-end 37-bp mRNA sequencing was performed on Illumina HiSeq2000 platform. Quality of sequencing was assessed using FastQC software. Raw reads in fastq format were collected and aligned to the mouse genome (mm10 version) using STAR 2.6 algorithm. Gene quantification was performed using HTSeq and differential expression analysis was performed using edgeR package. Results: We defined kidney-specific molecular signatures of the murine lupus transcriptome that mirrors nephritis-specific transcriptome alterations in human SLE. Conclusions: By the use of the mouse kidney-specific transcriptome and through training of a large whole-blood RNA-sequencing dataset of SLE patients, we developed and validated an algorithm that predicts patients with active LN from SLE patients without LN and suggest vigilance in the monitoring of these patients and potential enrollment in LN prevention studies.

2022-10-01 | GSE186367 | GEO

Expression data from lupus NZB/W and NZW/BXSB mouse prenephritic kidneys

Project description:We defined the shared and unique features of systemic lupus erythematosus (SLE) nephritis in 2 mouse models of proliferative renal disease. We identified shared inflammatory mechanisms of SLE nephritis that can be therapeutically targeted. Some common mechanisms are shared with non-immune-mediated renal diseases, suggesting that new strategies to prevent tissue hypoxia and remodeling may be useful in SLE nephritis.

2014-12-31 | GSE44691 | GEO

Comparison of Renal Transcriptome Profiles in Patients with Active Lupus Nephritis Reveals Possible New Mechanisms of Disease Progression

Project description:To identify factors that influence the progression of lupus nephritis (LN), we performed RNA sequencing on renal biopsy samples obtained from patients with active LN. The renal biopsy pathology followed the classification of the International Society of Nephrology and Renal Pathology Society (ISN/RPS) for 21 lupus nephritis patients: 2 in Class II, 3 in Class III, 10 in Class IV, 5 in Class V, and 1 patient with mixed type LN. The duration of disease from onset of systemic lupus erythematosus (SLE) to the onset of lupus nephritis was 26 months. Proteinuria was 2.5 (g/gCr or g/24hr), estimated Glomerular Filtration Rate (eGFR) was 72.9 (ml/min/1.73 m2), Index of activity was 5, and Index of chronicity was 3. Among different gene expression variations, the type I interferon (IFN) signature showed high expression in patients with shorter disease duration, preserved eGFR, and lower Index of chronicity. The type I IFN signature contributes to fibrosis in the tubulointerstitial space and worsens chronic lesions. Early control of the type I IFN signature may limit disease progression. Our results reveal a potential molecular mechanism for active LN and the link between functional and structural changes and differential gene expression observed in patients with early-stage LN.

2025-12-31 | GSE239576 | GEO

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