PRMT1 Modulates Processing of Asthma-Related Primary MicroRNAs (Pri-miRNAs) into Mature miRNAs in Lung Epithelial Cells

Abstract Protein arginine methyltransferase-1 (PRMT1) is an important epigenetic regulator of cell function and contributes to inflammation remodeling in asthma a type–specific manner. Disease-specific expression patterns microRNAs (miRNA) are associated with chronic inflammatory lung diseases, including asthma. The de novo synthesis miRNA depends on the transcription primary (pri-miRNA) transcript. This study assessed role PRMT1 pri-miRNA mature process epithelial cells. Human airway cells, BEAS-2B, were transfected plasmid pcDNA3.1-PRMT1 for 48 h. Expression profiles determined by small RNA deep sequencing. Comparing these miRNAs datasets microarrays from five patients (Gene Omnibus dataset), 12 identified that related overexpression or knockdown modulated asthma-related their pri-miRNAs. Coimmunoprecipitation showed formed complex STAT1 RUNX1 thus acted as coactivator, stimulating Stimulation TGF-?1 promoted interaction RUNX1, thereby upregulating two miRNAs: let-7i miR-423. Subsequent chromatin immunoprecipitation assays revealed binding PRMT1/STAT1 PRMT1/RUNX1 coactivators (pri-let-7i) miR (pri-miR) 423 promoter was critical pri-let-7i pri-miR-423 transcription. describes novel coactivator which essential cells might be relevant epithelium dysfunction