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. 2023 Jan 27;12(3):422. doi: 10.3390/cells12030422

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© 2023 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Diagram showing the possible molecular mechanism for the restoration of the BBB integrity by imatinib. Signaling pathways of Abl, CRKL and their relationship with endothelial junction and glycocalyx formation in the normal control BBB (A) and in the 22q11.DS BBB (B), in which haploinsufficiency of CRKL leads to lower level of unphosphorylated (active form) CRKL and induces interference with tight junctions and glycocalyx formation; (C) Inhibition of Abl kinase activity by imatinib increases the level of active form CRKL proteins and their interactions with p130Cas proteins to restore tight junctions and glycocalyx close to the control level.