Abstract：
:Vascular endothelial (VE)-cadherin homophilic adhesion controls endothelial barrier permeability through assembly of adherens junctions (AJs). We observed that loss of VE-cadherin-mediated adhesion induced the activation of Src and phospholipase C (PLC)γ2, which mediated Ca(2+) release from endoplasmic reticulum (ER) stores, resulting in activation of calcineurin (CaN), a Ca(2+)-dependent phosphatase. Downregulation of CaN activity induced phosphorylation of serine 162 in end binding (EB) protein 3. This phospho-switch was required to destabilize the EB3 dimer, suppress microtubule (MT) growth, and assemble AJs. The phospho-defective S162A EB3 mutant, in contrast, induced MT growth in confluent endothelial monolayers and disassembled AJs. Thus, VE-cadherin outside-in signaling regulates cytosolic Ca(2+) homeostasis and EB3 phosphorylation, which are required for assembly of AJs. These results identify a pivotal function of VE-cadherin homophilic interaction in modulating endothelial barrier through the tuning of MT dynamics.
journal_name
Mol Celljournal_title
Molecular cellauthors
Komarova YA,Huang F,Geyer M,Daneshjou N,Garcia A,Idalino L,Kreutz B,Mehta D,Malik ABdoi
10.1016/j.molcel.2012.10.011subject
Has Abstractpub_date
2012-12-28 00:00:00pages
914-25issue
6eissn
1097-2765issn
1097-4164pii
S1097-2765(12)00864-7journal_volume
48pub_type
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