Event Title

Role of N-cadherin Adhesion Mediated Signaling in Regulating Stability of VE-cadherin Adhesions Role of N-cadherin Adhesion Mediated Signaling in Regulating Stability of VE-cadherin Adhesions and Permeability Endothelial Barrier Function

Session Number

C28

Advisor(s)

Yulia Komarova, University of Illinois at Chicago
Kevin Kruse, University of Illinois at Chicago
Asrar Malik, University of Illinois at Chicago

Location

B-125 Tellabs

Start Date

28-4-2016 11:05 AM

End Date

28-4-2016 11:30 AM

Disciplines

Biology

Abstract

The endothelial monolayer lining the vascular system maintains tissue-fluid homeostasis through selective permeability. This permeability is a result of inter-endothelial junctions such as adherens junctions (AJs), which provide a physical attachment of endothelial cells by extracellular Vascular- Endothelial (VE)-cadherin adhesion. Stability of AJs is regulated by anchorage of VE-cadherin complexes of associated alpha-, beta-, and p120-catenins to the actin cytoskeleton in the Rho GTPasedependent manner. Neural (N)-cadherin form adhesion between endothelial and mural cells. Recent studies suggest that N-cadherin might also regulate endothelial barrier permeability. However, the complete mechanism of N-cadherin and VE-cadherin cross-interactions remains unknown. Data from the lab suggest that N-cadherin might control activity of RhoGTPases at AJs. Rho GTPases are molecular switches cycling between GTP- and GDP-bound states. This process is activated and inhibited by guanine-nucleotide exchange factors (GEFs) and GTPase-activating proteins. Trio is a RhoGEF consisting of two GEF domains. GEF1 activates Rac1 and RhoG while GEF2 activates RhoA. Trio needs Neuron Navigator (NAV)1 to activate Rac1. In this study, we investigated effect of NAV1 and Ncadherin signaling on recruitment of VE-cadherin to AJs. Our data show that both proteins are required for stabilization of VE-cadherin adhesion and restricting permeability.


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Apr 28th, 11:05 AM Apr 28th, 11:30 AM

Role of N-cadherin Adhesion Mediated Signaling in Regulating Stability of VE-cadherin Adhesions Role of N-cadherin Adhesion Mediated Signaling in Regulating Stability of VE-cadherin Adhesions and Permeability Endothelial Barrier Function

B-125 Tellabs

The endothelial monolayer lining the vascular system maintains tissue-fluid homeostasis through selective permeability. This permeability is a result of inter-endothelial junctions such as adherens junctions (AJs), which provide a physical attachment of endothelial cells by extracellular Vascular- Endothelial (VE)-cadherin adhesion. Stability of AJs is regulated by anchorage of VE-cadherin complexes of associated alpha-, beta-, and p120-catenins to the actin cytoskeleton in the Rho GTPasedependent manner. Neural (N)-cadherin form adhesion between endothelial and mural cells. Recent studies suggest that N-cadherin might also regulate endothelial barrier permeability. However, the complete mechanism of N-cadherin and VE-cadherin cross-interactions remains unknown. Data from the lab suggest that N-cadherin might control activity of RhoGTPases at AJs. Rho GTPases are molecular switches cycling between GTP- and GDP-bound states. This process is activated and inhibited by guanine-nucleotide exchange factors (GEFs) and GTPase-activating proteins. Trio is a RhoGEF consisting of two GEF domains. GEF1 activates Rac1 and RhoG while GEF2 activates RhoA. Trio needs Neuron Navigator (NAV)1 to activate Rac1. In this study, we investigated effect of NAV1 and Ncadherin signaling on recruitment of VE-cadherin to AJs. Our data show that both proteins are required for stabilization of VE-cadherin adhesion and restricting permeability.