A specific role for endothelial EPLIN-isoform-regulated actin dynamics in neutrophil transmigration.

ABSTRACT: Proinflammatory cytokines such as TNF-α or IL-1β activate the endothelium promoting leukocyte transendothelial migration (TEM) via expression of cell adhesion molecules (CAM) and cause actin remodelling. However, the function of endothelial actin remodelling in TEM remains elusive, despite its involvement in the formation of docking structures, diapedesis pores and pore resealing. Here, we establish EPLIN-isoforms, EPLIN-β and EPLIN-α, as differential regulators of TNF-α-inducedactin-remodelling significantly affecting TEM. We find EPLIN-β-induced stress fiber formation upon TNF-α-treatment weakens endothelial junctions, upregulates junctional dynamics and facilitates intercellular gaps for TEM. Increased junctional dynamics involves branched actin filaments under the control of EPLIN-α, i

SUBMITTER: Aldirawi M 

PROVIDER: S-EPMC12053001 | biostudies-literature | 2025 May

REPOSITORIES: biostudies-literature