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. 2018 Apr 26;8:6618. doi: 10.1038/s41598-018-24954-3

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© The Author(s) 2018

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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Reactivation of cell cycle in hiPSC-CMs with S1P and LPA is dependent on ERK signaling. (A) Luciferase luminescence intensity after transfection of day 30 hiPSC-CMs with TOPFlash Wnt signaling pathway activity reporter and 2-hour treatment with CHIR, S1P/LPA or both. The data shown represents fold increase over DMSO control. (B) Quantification of kinase assays illustrating alterations in hiPSC-CM kinome phosphorylation in response to 0, 5, 10, and 30-minute S1P/LPA treatment. Data expressed as means ± SEM. *indicates P < 0.05. (C) Representative kinase assay conducted in day 30 hiPSC-CMs treated with and without small molecule MEK inhibitor trametinib, with and without S1P/LPA (10 μM each). Spots corresponding to ERK phosphorylation and antibody control are labeled. (D) Immunofluorescence for cardiac troponin T (TnT) (green), ki67 (red) and nuclear DNA (blue) in day 30 hiPSC-CMs treated with S1P and LPA in the presence or absence of MEK inhibitor trametinib. (E) Quantification of the percentages of ki67 positive cardiomyocytes (CMs) in (D). *indicates P < 0.001. (F) Immunofluorescence for cardiac troponin T (TnT) (green), ki67 (red) and nuclear DNA (blue) in day 30 hiPSC-CMs treated with bioactive lipid S1P in the presence or absence of 5 μM S1P receptor antagonist VPC23019. (G) Quantification of the percentages of ki67 positive CMs after S1P treatments with or without 5 μM VPC23019. (H) Model illustrating the link between bioactive lipids and the canonical MAPK/MEK/ERK signaling pathway in differentiated hiPSC-CMs. N=4.