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Identification of key miRNAs and their targets in peripheral blood mononuclear cells of IgA nephropathy using bioinformatics analysis.


ABSTRACT:

Background

Currently, renal biopsy is the gold standard for clinical diagnosis and evaluation the degrees of IgA nephropathy. However, renal biopsy is an invasive examination and not suitable for long-term follow-up IgA nephropathy. The activation of peripheral blood mononuclear cells (PBMCs) are related to IgA nephropathy, but the key molecular marker and target of PBMCs for evaluating the progression and prognosis of IgA nephropathy is still unclear.

Methods

We downloaded gene expression omnibus series 25590 (GSE25590) datasets, of which PBMCs from IgA nephrology (IgAN) and healthy patients, from the gene expression omnibus (GEO) database. Differentially expressed miRNAs (DEMs) between IgAN and healthy patients were identified. The Funrich software was used to predict the differentially expressed genes (DEGs). Gene ontology (GO) and kyoto encyclopedia of genes and genomes (KEGG) analyzes of overlapping genes were analyzed at the function level on DAVID 6.8. We used search Tool for the retrieval of interacting genes (STRING) online database constructed the protein-protein interaction (PPI) network. Then we further analyzed the hub genes by Cytoscape software and the hub miRNA by TargetScan.

Results

We identified 418 DEMs from the GSE25590 datasets. The upstream transcription factors SP1 regulates most DEMs. According to the GO and KEGG results, the DEGs were enriched in the MAPK signaling pathway and small GTPase mediated signal transduction. SYN1, SYT4, RBFOX1, KCNC1, VAMP2, FBXO11, ASB9, SYT9, KLHL5, and KRAS were identified as hub genes. Hsa-miR-532-5p, hsa-miR-92a, hsa-miR-328, hsa-miR-137, hsa-miR-153, hsa-miR-9-5p, hsa-miR-140-5p, hsa-miR-217, hsa-miR-155, and hsa-miR-212 were predicted as hub miRNAs.

Conclusions

The DEMs and DEGs re-analysis provided potential key genes and hub miRNA of PMBCs, which may help to monitor the happening and prognosis of IgAN.

SUBMITTER: Liu L 

PROVIDER: S-EPMC8257889 | biostudies-literature |

REPOSITORIES: biostudies-literature

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