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. 2022 Feb 11;16:814867. doi: 10.3389/fncel.2022.814867

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Copyright © 2022 Xu, Chen, Fu, Yang, Yang, Huo, Tan, Chen and Wang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Interleukin-17A disrupts TJs and AJs by inhibiting PRTN3/PAR-2 axis. (A) The qPCR analysis of ZO-1, Occludin, Claudin-5, and VE-Cadherin extracted from IL-17A untreated hBMECs and IL-17A treated hBMECs with or without the overexpression of PRTN3. GAPDH was used as the internal reference. Data were presented as mean ± SD from three independent experiments. ***p < 0.001 by one-way ANOVA analysis. (B) Western blot of ZO-1, Occludin, Claudin-5 and VE-Cadherin extracted from IL-17A untreated hBMECs and IL-17A treated hBMECs with or without overexpression of PRTN3. β-Actin was used as the loading control. (C) The qPCR analysis of ZO-1, Occludin, Claudin-5, and VE-Cadherin extracted from IL-17A untreated hBMECs and IL-17A treated hBMECs with or without PAR-2 agonist AC-55541. GAPDH was used as the internal reference. Data were presented as mean ± SD from three independent experiments. ***p < 0.001 by one-way ANOVA analysis. (D) Western blot of ZO-1, Occludin, Claudin-5, and VE-Cadherin extracted from IL-17A untreated hBMECs and IL-17A treated hBMECs with or without PAR-2 agonist AC-55541. β-Actin was used as the loading control. (E) TEER changes of the IL-17A untreated hBMECs and IL-17A treated hBMECs with or without PAR-2 agonist AC-55541 monitored by the ECIS system. Data were collected and presented as mean ± SD from three replicated wells at each time point.