Myosin light chain phosphorylation facilitates monocyte transendothelial migration by dissociating endothelial adherens junctions

Abstract

Our studies suggest that monocyte-induced phosphorylation of MLC in ECs enhances TEM of monocytes through dissociation of EC adherens junctions.

Stretch-induced human myometrial cytokines enhance immune cell recruitment via endothelial activation

“…11,56,57 Leukocytes can undertake two routes during TEM: transcellular (through cytoplasm) or paracellular (between adjacent ECs) pathways. [57][58][59] In this study, we demonstrated that myometrial cytokines (irrespective of stretch) augment vascular permeability, which allow selective yet specific passage of blood cells and macromolecules.…”

Integrin α2β1 Mediates Tyrosine Phosphorylation of Vascular Endothelial Cadherin Induced by Invasive Breast Cancer Cells

“…Tumor cell invasion may closely resemble leukocyte trafficking, in which the endothelium acts as a barrier and greatly reduces invasion rates (13). Recently, we identified signal transduction pathways that regulate the transendothelial migration (TEM) of monocytes (14). In the present study, we determined that the attachment of invasive breast cancer cells (MDA-MB-231 cells) to endothelial cells leads to the disorganization of adherens junction structure and Tyr phosphorylation of VE-cad.…”

“…After incubation with viral particles for 48 h, the cells were assessed for the expression of the transduced genes. The efficacy of all recombinant adenoviruses was previously tested (14).…”

“…Cells-We recently showed that the interaction of monocytes with endothelial cells leads to Tyr phosphorylation of VE-cad and disruption of endothelial adherens junctions (14). To determine if the interaction of breast cancer cells with endothelial cells leads to similar effects on endothelial adherens junctions, invasive breast cancer cells (MDA-MB-231) were added to a monolayer of HUVECs.…”

Blood cells and endothelial barrier function

“…This results in the recruitment of Src to VE-cadherin and phosphorylation, the dissociation of VE-cadherin/b-catenin complex, and ultimately gap junction formation. 114 There is also evidence that supports a protective role for monocytes in the maintenance of endothelial barrier function. As described above for neutrophils, 96 it has been reported that microparticles released from activated monocytes enhance the tightness of endothelial cell monolayers after exposure to bacterial endotoxin.…”