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. 2024 Nov 14;14:28012. doi: 10.1038/s41598-024-77776-x

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, 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 licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by-nc-nd/4.0/.

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Fig. 1 — Cigarette smoke extract alters PP2A activity and distribution within endothelial cells. (A) Human microvascular lung endothelial cells (HLMVEC) were grown to 80% confluence in 6-well plates and treated with 5% CSE for 10 min, 30 min, 1, 6, 12 and 24 h. PP2A activity assays were conducted on lysate protein isolated from the cells at baseline and after 5% CSE treatment. (B) PP2A activity assays were conducted on cytosolic, nuclear, cytoskeletal and membrane protein fractions of HLMVECs treated with and without 5% CSE for 24 h. (C) Immunoblots for the catalytic subunit of PP2A (PP2AC) were conducted on membrane fractions of HLMVECs treated with control media or 5% CSE for 24 h. Actin immunoblots were conducted on membrane fractions as a loading control.