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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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Cocaine treatment activates MMP-9 and MMP-2. (A) Schematic representation of the steps and enzymes involved the biochemical degradation of ECM-associated collagen. (B) HBMECs were treated with a range of concentrations of cocaine for 18–24 h and the culture supernatants were used as the source of MMP-9 and MMP-2 activity by zymography. (C,D) Densitometry analysis of MMP-9 (C) and MMP-2 (D) activity in HBMECs from three independent experiments. (E) Effects of MMP inhibition on cocaine-mediated increased permeability. The HMBEC monolayer in the transwell were treated with cocaine (50 μM) or cocaine + the MMP inhibitor GM6011. Then FITC-permeability 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 to cocaine and GM6011-treated samples by **P < 0.05.