TY - JOUR
T1 - N-cadherin levels in endothelial cells are regulated by monolayer maturity and p120 availability.
AU - Ferreri, Deana M.
AU - Minnear, Fred L.
AU - Yin, Taofei
AU - Kowalczyk, Andrew P.
AU - Vincent, Peter A.
N1 - Funding Information:
This work was supported by grants HL-77870 to P.A.V., HL-68079 to F.L.M., and AR-050501 to A.P.K. from the National Institutes of Health. Address correspondence to Peter A. Vincent, PhD, Professor, Center for Cardiovascular Sciences, Albany Medical College, 47 New Scotland Avenue, Albany, NY 12208, USA. E-mail: [email protected]
PY - 2008/11
Y1 - 2008/11
N2 - Endothelial cells (ECs) express VE-cadherin and N-cadherin, and recent data suggest that VE-cadherin levels are dependent on N-cadherin expression. While investigating changes in N-cadherin levels during endothelial monolayer maturation, the authors found that VE-cadherin levels are maintained in ECs despite a decrease in N-cadherin, suggesting that VE-cadherin levels may not depend on N-cadherin. Knockdown of N-cadherin did not affect VE-cadherin levels in ECs with low endogenous N-cadherin expression. Surprisingly, however, knockdown of N-cadherin in ECs with high endogenous N-cadherin expression increased VE-cadherin levels, suggesting an inverse relationship between the two. This was further supported by a decrease in VE-cadherin following overexpression of N-cadherin. Experiments in which p120, a catenin that binds N- and VE-cadherin, was knocked down or overexpressed indicate that these two cadherins compete for p120. These data demonstrate that VE-cadherin levels are not directly related to N-cadherin levels but may be inversely related due to competition for p120.
AB - Endothelial cells (ECs) express VE-cadherin and N-cadherin, and recent data suggest that VE-cadherin levels are dependent on N-cadherin expression. While investigating changes in N-cadherin levels during endothelial monolayer maturation, the authors found that VE-cadherin levels are maintained in ECs despite a decrease in N-cadherin, suggesting that VE-cadherin levels may not depend on N-cadherin. Knockdown of N-cadherin did not affect VE-cadherin levels in ECs with low endogenous N-cadherin expression. Surprisingly, however, knockdown of N-cadherin in ECs with high endogenous N-cadherin expression increased VE-cadherin levels, suggesting an inverse relationship between the two. This was further supported by a decrease in VE-cadherin following overexpression of N-cadherin. Experiments in which p120, a catenin that binds N- and VE-cadherin, was knocked down or overexpressed indicate that these two cadherins compete for p120. These data demonstrate that VE-cadherin levels are not directly related to N-cadherin levels but may be inversely related due to competition for p120.
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U2 - 10.1080/15419060802440377
DO - 10.1080/15419060802440377
M3 - Article
C2 - 18979298
AN - SCOPUS:58149330508
SN - 1541-9061
VL - 15
SP - 333
EP - 349
JO - Cell Adhesion and Communication
JF - Cell Adhesion and Communication
IS - 4
ER -