Specific regulation of PRMT1 expression by PIAS1 and RKIP in BEAS-2B epithelia cells and HFL-1 fibroblasts in lung inflammation

• DOI: 10.1038/srep21810
• Publication Date: 2016-02-25T10:10:10Z
• Authors: Li Liu; Qingzhu Sun; Rujuan Bao; Michael Roth; Bo Zhong; Xi Lan; Jia Tian; Qirui He; Dongmin Li; Jian Sun; Xudong Yang; Shemin Lu
• Keywords: 0301 basic medicine; Protein-Arginine N-Methyltransferases; Binding Sites; Blotting, Western; Interleukin-1beta; NF-kappa B; Epithelial Cells; Phosphatidylethanolamine Binding Protein; Pneumonia; Fibroblasts; Protein Inhibitors of Activated STAT; Article; 03 medical and health sciences; Microscopy, Fluorescence; A549 Cells; Cyclooxygenase 2; Humans; Immunoprecipitation; Interleukin-4; Phosphorylation; Promoter Regions, Genetic; Lung; Cells, Cultured

Abstract Protein arginine methyltransferase 1 (PRMT1) catalyzes methylation of histones and other cellular proteins, thus regulates gene transcription protein activity. In antigen-induced pulmonary inflammation (AIPI) PRMT1 was up-regulated in the epithelium, while chronic AIPI, increased shifted to fibroblasts. this study we investigated cell type specific regulatory mechanism PRMT1. Epithelial cells fibroblasts were stimulated with IL-4 or IL-1β. Gene expression determined by RT-qPCR, immunohistochemistry staining Western blotting. Signaling pathway inhibitors, siRNAs shRNA used determine The results showed that through STAT6 signaling epithelial cells, IL-1β regulated NF-κB NF-kB inhibitor RKIP highly expressed blocked induced up-regulation; PIAS1 suppressed expression. Furthermore, release which conclusion, proteins Thus structural lung asthma can be considered as potential target for new therapeutic intervention.