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. 2021 Jan 21;12(1):109. doi: 10.1038/s41419-020-03385-x

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© The Author(s) 2021

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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Fig. 4 — A Primary BMDMs subtypes were stimulated by VEGF-C in vitro, and then the expression of macrophage activation markers (iNOS for M1, arginase for M2) and lymphatic vessel markers (Prox-1, LYVE-1, and podoplanin) were measured by western blotting. B In vitro, primary BMDMs were analyzed by immunofluorescence for iNOS, LYVE-1, and podoplanin expression after VEGF-C stimulation or control treatment (CTRL) (400×). C M1 macrophages were treated with VEGF-C, siRNA for VEGF-C (Si-VEGF-C), and the VEGFR3 inhibitor SAR131675 (SAR-23/46 nM), and then the protein expression of iNOS, arginase, and lymphatic vessel markers (LYVE-1 and Prox-1) was measured.