Fibrin-VLDL Receptor-Dependent Pathway Promotes Leukocyte Transmigration by Inhibiting Src Kinase Fyn and is a Target for Fibrin β15-42 Peptide.

ABSTRACT: According to the current view, binding of fibrin degradation product E₁ fragment to endothelial VE-cadherin promotes transendothelial migration of leukocytes and thereby inflammation, and fibrin-derived β15-42 peptide reduces leukocyte transmigration by competing with E₁ for binding to VE-cadherin and, in addition, by signaling through Src kinase Fyn. However, the very low affinity of β15-42 to VE-cadherin raised a question about its ability to inhibit E₁-VE-cadherin interaction. Further, our previous study revealed that fibrin promotes leukocyte transmigration through the very-low-density lipoprotein (VLDL) receptor (VLDLR)-dependent pathway and suggested a possible link between the inhibitory properties of β15-42 and this pathway. To test such a link and

SUBMITTER: Yakovlev S 

PROVIDER: S-EPMC7179994 | biostudies-literature | 2019 Nov

REPOSITORIES: biostudies-literature