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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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Inhibition of miR-352 enhances arteriogenesis and promotes flow restoration in rat hind limbs. Ligature: the ligature-only side; Shunt: the AV shunt side; antagomir-352: rats infused with antagomirs targeting miR-352 through an osmotic mini pump connected to the proximal region of the occluded femoral artery; and antagomir-cont: control antagomir. (A) Postmortem angiograms of rat hind limbs on day 7 after infusion. Antagomir-352 treatment resulted in an increase in the number of collateral vessels (arrows) as compared to antagomir-cont treatment. This increase is similar to the number of collateral vessels observed following shunt treatment. (***P < 0.001, **P < 0.01, n = 5). (B) Cell proliferation was detected by Ki67 immunostaining in collateral vessels from different groups. Green fluorescence for Ki67, red for F-actin, blue for nuclei. Notably, Ki67-positive cells were more numerous in collaterals treated with antagomir-352 than in the control side, which is similar to what is observed following shunt treatment (**P < 0.01, n = 5). (C) Flow ratio of rat hind limbs at day 7 after antagomir-352 infusion and fluorescence microspheres administration in adductor muscles. Antagomir-352 treatment resulted in a significant increase in collateral flow, compared to antagomir-cont treatment. This increase is similar to that observed following shunt treatment (**P < 0.01, ***P < 0.001, n = 5). Red fluorescence for the fluorescence microspheres, and green for F-actin. The number of fluorescence microspheres was higher in the antagomir-352-treated and AV shunt-side muscles.