Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2021 Oct 4;11(4):20458940211049002. doi: 10.1177/20458940211049002

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2021

Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

PMC Copyright notice

Fig 2. — EVL involvement in regulation of thrombin-induced endothelial cell barrier dysfunction. HPAEC were transduced with either myc-EVL or GFP (a–c) or transfected with a siRNA against EVL or a non-targeting sequence (d–f). EC were treated with the vascular barrier-disrupting agent thrombin and TEER followed over time. (a). HPAEC cells over-expressing myc-EVL showed a lower electrical resistance in response to thrombin (0.25 and 0.50 units/ml) in comparison to GFP-transduced cells indicating that that EVL stabilized the vascular barrier upon thrombin treatment. (b) Stabilization is indicated by the reduction in thrombin-induced barrier disruption in EVL-transduced cells. Responses to thrombin was dose-dependent (n = 4, **=p < 0.01). Over-expression of the EVL-myc and GFP was confirmed using Western blotting against myc and GFP (c). Lane 1. GFP and Lane 2. myc-EVL-transduced cells. Vinculin was used as the loading control. (d) HPAEC transfected with EVL siRNA showed a greater drop in electrical resistance in response to thrombin indicating increased vascular leak and underscoring the role of EVL in vascular barrier stabilization. (e) The increased leakage is highlighted by the greater decrease in resistance of EVL siRNA treated cells (n = 4, **=p < 0.01). The efficiency of knockdown was verified using Western blotting against EVL and vinculin was used as the loading control (f). Lane 1 Non-targeting and Lane 2. EVL siRNA transfected cells. Quantification of band density is shown in (c) and (f).