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. 2020 Jul 7;10:11186. doi: 10.1038/s41598-020-68019-w

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© The Author(s) 2020

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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Exposure to PGE2 disrupts pericytes and damages vessel wall integrity. In normal condition, pericytes are closely interacting and communicating with ECs via adherens junctions (N-cadherin), gap junctions (Cx43), and cell adhesion to basement membrane extracellular matrix (yellow). The exposure to PGE2-high environment in pathological conditions, such as colon cancer, disrupts normal pericyte function, which in turn causes disruption of the EC lining of blood vessel wall. The use of EP1 and EP4 inhibitors can restore the vascular damages induced by PGE2.