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. 2019 Feb 22;9:2567. doi: 10.1038/s41598-018-37495-6

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© The Author(s) 2019

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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Prolidase regulates cocaine-induced permeability through endothelial cell barrier. (A) Prolidase expression was knocked-down by siRNA-based method and confirmed by immunoblot analysis. (B) Cocaine (50 μM) was added to the HMBEC monolayer in the trans-well without or with prolidase knock-down conditions. Then FITC-permeability in these trans-wells was measured. Data represents the mean ± SEM of at least three determinations. *P < 0.05 represents statistical comparison of untreated and cocaine-treated samples, whereas that of cocaine-treated sample with and without prolidase knock-down is depicted by **P < 0.05.