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. 2017 Jul 27;7:6643. doi: 10.1038/s41598-017-06910-9

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© The Author(s) 2017

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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Effect of miR-352 overexpression or inhibition on angiogenesis in cultured rat aorta endothelial cells (RAECs). RAECs were transfected with either miR-352 mimic, miR-352 inhibitor or the respective negative controls: mimic control/inhibitor control. (A) Transfected cells were cultured on Matrigel, and the cumulative sprout length and branch points of capillary-like structures were measured after 6 hours. miR-352 mimic attenuated angiogenic tube formation, whereas inhibition of miR-352 had a stimulatory effect. (***P < 0.001, n = 3). (B) Stained migratied transfected cells on the bottom side of the Transwell chamber after 24 hours. miR-352 mimic attenuated cell migration, whereas inhibition of miR-352 promoted cell migration. (***P < 0.001, n = 3). (C) Proliferation of transfected cells was examined by Ki67 immunostaining. Green for Ki67, and blue for nuclei. miR-352 mimic attenuated cell proliferation, whereas miR-352 inhibitor promoted cell proliferation (*P < 0.05, n = 3).