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- W2765097306 abstract "Abstract Changes in miRNA expression of glomerular capillaries during antibody-mediated rejection (ABMR) are poorly understood and could contribute to the deleterious inflammation and fibrosis of ABMR via suppression of target genes. A better understanding could lead to novel diagnostic tools and reveal novel therapeutic targets. We explored deregulated miRNAs in an glomeruloendothelial in vitro model of ABMR due to class I human leukocyte antigen (HLA) with and without complement activation. We studied a set of 16 promising candidate miRNAs in microdissected glomeruli a confirmation set of 20 human transplant biopsies (DSA+) compared to 10 matched controls without evidence for ABMR. Twelve out of these 16 glomerulocapillary miRNAs could successfully be confirmed as dysregulated in vivo with 10 upregulated (let-7c-5p, miR-28-3p, miR-30d-5p, miR-99b-5p, miR-125a-5p, miR-195-5p, miR-374b-3p, miR-484, miR-501-3p, miR-520e) and 2 downregulated (miR29b-3p, miR-885-5p) in DSA+ vs. controls. A random forest analysis based on glomerular miRNAs identified 18/20 DSA+ and 8/10 controls correctly. This glomerulocapillary miRNA signature associated with HLA class I-DSA could improve our understanding of ABMR and be useful for diagnostic or therapeutic purposes." @default.
- W2765097306 created "2017-11-10" @default.
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- W2765097306 date "2017-11-06" @default.
- W2765097306 modified "2023-09-23" @default.
- W2765097306 title "Glomerulocapillary miRNA response to HLA-class I antibody in vitro and in vivo" @default.
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- W2765097306 doi "https://doi.org/10.1038/s41598-017-14674-5" @default.
- W2765097306 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5673998" @default.
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- W2765097306 hasPublicationYear "2017" @default.
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