TNF-α induces VE-cadherin-dependent gap/JAIL cycling through an intermediate state essential for neutrophil transmigration.

ABSTRACT: Inflammatory endothelial phenotypes describe distinct cellular patterns essential for controlling transendothelial migration of leukocytes (TEM). While TNF-α-induced CAM expression mediates leukocyte interaction, the role of a potential inflammatory morphological phenotype (IMP) - characterized by barrier-function decrease and shape-change in TEM - remains unclear. This study identifies the TNF-α-induced IMP as indispensable for neutrophil TEM, while regulating barrier-function. The TNF-α-induced IMP progresses through two states: an intermediate state that transiently enhances barrier function via MLC-dephosphorylation, junctional actin recruitment and VE-cadherin linearization, protecting the monolayer from collapse; while the subsequent development of the IMP requires MLC rephosphorylat

SUBMITTER: Kipcke JP 

PROVIDER: S-EPMC12454053 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature