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. 2020 Jan 15;10:413. doi: 10.1038/s41598-019-57200-5

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© The Author(s) 2020

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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Analysis of ¹³C-labeled metabolite content derived from [1,2,3-¹³C₃]glucose indicates TGF-β increases glycolysis in PASMCs. (a,b) ¹³C₃- and ¹³C₂-Labeled lactate (M + 3 lactate is derived from glycolysis and M + 2 lactate is derived from pentose shunt metabolism) in the supernatant of (a) control or (b) diseased PASMCs, treated with or without TGF-β. (c,d) ¹³C₃- and ¹³C₂-Labeled lactate in the supernatant of (c) control or (d) diseased PAECs, treated with or without TGF-β. (N = 5 samples per group, from 5 different control and 5 different disease subjects; paired t-test; *P < 0.05).