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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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miR-352 regulates endothelial tube formation and cell proliferation in cultured RAECs by targeting the IGF2R gene. (A) Effect of miR-352 inhibitor + siIGF2R (IGF2R siRNA); miR-352 inhibitor + siNC (a scrambled siRNA); siIGF2R + inhibitor cont; or siNC + inhibitor cont on endothelial tube formation (***P < 0.001, n = 3). (B) Effect of the miR-352 inhibitor + siIGF2R (IGF2R siRNA); miR-352 inhibitor + siNC (a scrambled siRNA); siIGF2R + inhibitor cont or siNC + inhibitor cont on RAEC proliferation was detected by Ki67 immunofluorescence. Specific fluorescence in green, and nuclei are labelled in blue. Notably, treatment with miR-352 inhibitor + siIGF2R or inhibitor cont + siIGF2R significantly reduced both endothelial tube formation and cell proliferation in cultured RAECs as compared to treatment with miR-352 inhibitor + siNC or inhibitor + siNC, respectively, indicating that IGF2R is a miR-352 target in RAECs (***P < 0.001, *P < 0.05, n = 3).