Integrated analysis of microRNA regulation and its interaction with mechanisms of epigenetic regulation in the etiology of systemic lupus erythematosus
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Fecha
2019
Autores
Navarro Quiroz, Elkin
Navarro Quiroz, Roberto
Pacheco Lugo, Lisandro
Aroca Martínez, Gustavo
Gómez Escorcia, Lorena
Gonzalez Torres, Henry
Cadena Bonfanti, Andres
Marmolejo, Maria del Carmen
Sanchez, Eduardo
Villarreal Camacho, Jose Luis
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Editor
Public Library of Science
Facultad de Ciencias Básicas y Biomédicas
Facultad de Ciencias Básicas y Biomédicas
Resumen
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, hsamiR-
374a-5p, hsa-miR-34a-5p, hsa-miR-31-5p, and hsa-miR-1-3p.
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Palabras clave
MicroRNAs, Systemic lupus erythematosus, DNA methylation, Post-translational modification, Epigenetics, Transcription factors, Gene regulation