Integrated analysis of microRNA regulation and its interaction with mechanisms of epigenetic regulation in the etiology of systemic lupus erythematosus
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Author/sNavarro Quiroz, Elkin; Navarro Quiroz, Roberto; Pacheco Lugo, Lisandro; Aroca Martínez, Gustavo; Gómez Escorcia, Lorena; González Torres, Henry; Cadena Bonfanti, Andrés; Marmolejo, María del Carmen; Sánchez, Eduardo; Villarreal Camacho, José Luis; Lorenzi, Hernan; Torres, Augusto; Navarro, Kelvin Fernando; Navarro Rodriguez, Pablo; Villa, Joe Luis; Fernández Ponce, Cecilia Matilde
DepartmentBioquímica y Biología Molecular, Microbiología, Medicina Preventiva, Salud Pública
SourcePLoS ONE 14(6): e0218116
The aim of this study was to identity in silico the relationships among microRNAs (miRNAs) and genes encoding transcription factors, ubiquitylation, DNA methylation, and histone modifications in systemic lupus erythematosus (SLE). To identify miRNA dysregulation in SLE, we used miR2Disease and PhenomiR for information about miRNAs exhibiting differential regulation in disease and other biological processes, and HMDD for information about experimentally supported human miRNA-disease association data from genetics, epigenetics, circulating miRNAs, and miRNA-target interactions. This information was incorporated into the miRNA analysis. High-throughput sequencing revealed circulating miRNAs associated with kidney damage in patients with SLE. As the main finding of our in silico analysis of miRNAs differentially expressed in SLE and their interactions with disease-susceptibility genes, post-translational modifications, and transcription factors; we highlight 226 miRNAs associated with genes and processes. Moreover, we highlight that alterations of miRNAs such as hsa-miR-30a-5p, hsa-miR-16-5p, hsa-miR-142-5p, and hsa-miR-324-3p are most commonly associated with post-translational modifications. In addition, altered miRNAs that are most frequently associated with susceptibility-related genes are hsa-miR-16-5p, hsa-miR-374a-5p, hsa-miR-34a-5p, hsa-miR-31-5p, and hsa-miR-1-3p.