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. 2017 Sep 5;7:10506. doi: 10.1038/s41598-017-11038-x

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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LY2157299 modulates TGF-β signalling after smoke exposure by decreasing Smad3 and p38 activation, thereby preserving CFTR and BK activities as well as ASL volume. (a) Schematic diagram showing LY2157299 (10 µM) effects on the TGF-β pathway (p38/HSP-27 and Smad3), activated by smoke exposure. (b) LY2157299 prevented smoke-induced Smad3 and HSP-27 phosphorylation at 2 h when compared to cells exposed to cigarette smoke alone. Below each quantification, a representative western blot is shown. Abbreviations are: S (Smoke) and LY (LY2157299). (c) LY2157299 improved CFTR and BK conductance at 2 h as well as ASL volume loss at 4 h after smoke exposure. ΔCFTR and ΔBK activity represent the difference of smoke exposed and air exposed cells, ΔSmoke + DMSO = Smoke + DMSO-exposed cells - average of control cells exposed to air + DMSO; ΔSmoke + LY = Smoke + LY2157299 - average of control cells exposed to air + LY. *Indicates p < 0.05 compared to control (6 h air exposure). All n ≥ 4 from at least 3 lungs.