N-cadherin coordinates AMP kinase-mediated lung vascular repair

Abstract

coordinates AMP kinase-mediated lung vascular repair.

Protein Interactions at Endothelial Junctions and Signaling Mechanisms Regulating Endothelial Permeability

“…An attractive hypothesis is that N-cadherin adhesion, which is involved in the recruitment of pericytes 90, 92 , also contributes to the assembly of TJs (although the mechanisms of this unknown, this idea deserves scrutiny). Another study demonstrating that N-cadherin adhesion-induced signaling contributes to the resolution of lung vascular injury through an AMP kinase dependent mechanism 103 is consistent with this concept.…”

VCAM-1 induces signals that stimulate ZO-1 serine phosphorylation and reduces ZO-1 localization at lung endothelial cell junctions

“…To examine leukocyte recruitment and adhesion molecules in allergic lung inflammation, we used the OVA mouse model because in this model, recruitment of eosinophil and lymphocytes is mediated by binding to VCAM‐1 . Endothelial cells express VCAM‐1 on the cell surface and in cell junctions and express angiomotin and VE‐cadherin in cell junctions; also, the junction molecule N‐cadherin can be induced on endothelial cells . OVA‐challenged mice had increased expression of VCAM‐1, angiomotin and N‐Cadherin by lung venule endothelial cells as compared to saline‐challenged lungs (Figs.…”

“…[45][46][47] Interestingly, asthmatic patient lung endothelial cells have increased angiomotin. 48 Lung endothelial cells also exhibit increased expression of N-Cadherin during endotoxin stimulation, 49 but it is not known whether allergic inflammation upregulates lung endothelial cell N-cadherin expression. Thus, whether induction of allergic inflammation or VCAM-1 signaling alters expression or localization of ZO-1, angiomotin, or N-cadherin in endothelial cells is not known.…”

Regulation of pulmonary endothelial barrier function by kinases

“…It was recently reported that N-cadherin coordinates AMPK-mediated lung vascular repair, since disruption of N-cadherin's intracellular domain caused translocation of AMPK away from the membrane and attenuated the AMPK-mediated restoration of barrier function in LPS-treated pulmonary endothelium. AMPK activation reversed the LPS-induced increase in vascular permeability, whereas N-cadherin inhibition inhibited the AMPK-mediated repair (110). Additionally, AMPK inhibits RhoA and RhoAassociated protein kinase (ROCK) activation (247).…”