Dataset Information

Urine proteomics in IgA nephropathy

ABSTRACT: we aimed at developing a urinary biomarker-based algorithm that predicts rapid disease progression in IgAN, thus enabling a personalized risk stratification.

INSTRUMENT(S): micrOTOF II

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Urine

DISEASE(S): Iga Glomerulonephritis

SUBMITTER: Martin Pejchinovski

LAB HEAD: Martin Pejchinovski

PROVIDER: PXD020288 | Pride | 2022-02-15

REPOSITORIES: Pride

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Publications

Urine proteomics for prediction of disease progression in patients with IgA nephropathy.

Rudnicki Michael M Siwy Justyna J Wendt Ralph R Lipphardt Mark M Koziolek Michael J MJ Maixnerova Dita D Peters Björn B Kerschbaum Julia J Leierer Johannes J Neprasova Michaela M Banasik Miroslaw M Sanz Ana Belen AB Perez-Gomez Maria Vanessa MV Ortiz Alberto A Stegmayr Bernd B Tesar Vladimir V Mischak Harald H Beige Joachim J Reich Heather N HN

Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 20211201 1

<h4>Background</h4>Risk of kidney function decline in immunoglobulin A (IgA) nephropathy (IgAN) is significant and may not be predicted by available clinical and histological tools. To serve this unmet need, we aimed at developing a urinary biomarker-based algorithm that predicts rapid disease progression in IgAN, thus enabling a personalized risk stratification.<h4>Methods</h4>In this multicentre study, urine samples were collected in 209 patients with biopsy-proven IgAN. Progression was define ...[more]

PMID: 33313853

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Project description:Non-optimal fetal environments resulting in low birth weight have epidemiologically been associated with a higher risk of adult diseases. In animal models, maternal undernutrition has successfully demonstrated that offspring owed increased risks for adult diseases. In mice, shorten life span was also demonstrated in offspring following maternal undernutrition. In the present study, we treated pregnant mice with 50% food restriction (FR), and performed global gene expression and promotor DNA methylation profiling on the fetal livers. Considering that effects of food restriction is opposite between before and after birth, we further searched genes which are regulated oppositely against adult calorie restriction (CR) and commonly against aging. Among searched genes, trib1 has already been demonstrated to contribute to a risk of cardiovascular disease, hypertriglyceridaemia and insulin resistance. The present result suggests that expression of trib1 is affected by maternal nutrition, and is one of the most responsible genes for developmental origins of metabolic syndrome. In addition, lepr was also down-regulated by maternal FR, suggested a potential role of this gene in induction of obesity and diabetes. Promotor DNA methylation profiling as well as gene expression profiling revealed that glucocorticoid receptor target genes were regulated by maternal FR. This finding supports previous studies that suggest an important role for glucocorticoid in developmental origins of metabolic syndrome. In the immune system, most of the genes related to interferon were down-regulated in their expression with up-regulation of their promoter DNA methylation. The profiling also suggested diminished NF-κB signalling. These results suggested that maternal FR affected development of the immune system. We presented here a list of genes responsible for developmental origins of health and disease, which were regulated oppositely against adult CR, and commonly against aging, and also affected their promotor DNA methylation. The present list hopefully contributes to prediction of risks for non communicable diseases, and also prediction of prenatal environment of nutrition from offspring materials. Here we carried out global gene expression profiling analysis on the fetal mouse liver following maternal 50% FR. Considering that opposite effects of nutrition between the fetus and adult, we further analyzed our fetal array data by comparing with data from their mothers, and array data on the effect of CR and aging in previous reports using adult rodent tissues. In addition, we performed global DNA methylation analysis using mouse promoter microarray, and compared the results with data of the gene expression analysis. Finally, we presented a list of candidate genes responsible for DOHaD.

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