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. 2019 Jan 17;9:160. doi: 10.1038/s41598-018-37232-z

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© The Author(s) 2019

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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An exogenous bacterial endotoxin (LPS) and an endogenous inflammatory cytokine (SAA) up-regulated Panx1 expression in macrophage (Mϕ) and monocyte (MC) cultures. Murine macrophage-like RAW264.7 cells (Panel a), differentiated human macrophages (Panel b), human peripheral blood mononuclear cells (MC, Panel c), or primary murine peritoneal macrophages (Panel d) were stimulated with crude LPS or SAA at indicated concentrations for indicated time periods, and the cellular Panx1 levels were measured by Western blotting (Panel a,b,c) or immunocytochemistry (Panel d), respectively. A house-keeping gene product β-actin was used as a loading control to estimate the relative Panx1/β-actin (P/A) ratio in macrophage or monocyte cultures.