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. 2016 Feb 25;6:21810. doi: 10.1038/srep21810

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Copyright © 2016, Macmillan Publishers Limited

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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In epithelial cells, IL-4 activated STAT6 signaling and then PRMT1 expression was up-regulated, while IL-1β increased RKIP and IκB expression and restrained the NF-κB signaling (A). In fibroblasts, up-regulated PIAS1 inhibit STAT6 signal pathway which is integral for IL-4 induced PRMT1 up-regulation, and IL-1β up-regulated PRMT1 expression via NF-κB signaling pathway (B). The mechanism explains why in acute asthma, the PRMT1 expression up-regulated in epithelium, while in chronic asthma, PRMT1 is up-regulated in fibroblasts.