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. 2018 Nov 9;8:16633. doi: 10.1038/s41598-018-34747-3

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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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Formation of F-actin stress fibers in differentiating NHCF-V is refractory to suppression by ASC-CMed. Representative immunofluorescence micrographs of human cardiac fibroblasts (NHCF-V) under stimulation with TGF-β1 or co-stimulation with TGF-β1 and FGF-2, both in FBM and ASC-CMed, for 5 days. Upon TGF-β1 stimulation, cells developed transcellular αSMA-expressing stress fibers (arrows). ASC-CMed did not inhibit the development of stress fibers. Blue: DAPI; Green: phalloidin; Red: αSMA. Scale reference: 100 μm.