Abstract:
:We have previously shown that Rap1 as well as its guanine nucleotide exchange factor Epac1 increases cell-cell junction formation. Here, we show that activation of Epac1 with the exchange protein directly activated by cAMP (Epac)-specific cAMP analog 8CPT-2'O-Me-cAMP (007) resulted in a tightening of the junctions and a decrease in the permeability of the endothelial cell monolayer. In addition, 007 treatment resulted in the breakdown of actin stress fibers and the formation of cortical actin. These effects were completely inhibited by siRNA against Epac1. In VE-cadherin knock-out cells Epac1 did not affect cell permeability, whereas in cells re-expressing VE-cadherin this effect was restored. Finally, the effect of Epac activation on the actin cytoskeleton was independent of junction formation. From these results we conclude that in human umbilical vein endothelial cells Epac1 controls VE-cadherin-mediated cell junction formation and induces reorganization of the actin cytoskeleton.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Kooistra MR,Corada M,Dejana E,Bos JLdoi
10.1016/j.febslet.2005.07.080keywords:
subject
Has Abstractpub_date
2005-09-12 00:00:00pages
4966-72issue
22eissn
0014-5793issn
1873-3468pii
S0014-5793(05)00949-Xjournal_volume
579pub_type
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