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This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: 297/5/C1168    most recent 00237.2009v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Andreeva, A. V. Articles by Voyno-Yasenetskaya, T. A. PubMed PubMed Citation Articles by Andreeva, A. V. Articles by Voyno-Yasenetskaya, T. A.

Vascular Biology

T-cadherin is located in the nucleus and centrosomes in endothelial cells

¹Department of Pharmacology, University of Illinois at Chicago, Chicago, Illinois; and ²Cardiology Research Center, Moscow, Russia

Submitted 1 June 2009 ; accepted in final form 31 August 2009

T-cadherin (H-cadherin, cadherin 13) is upregulated in vascular proliferative disorders and in tumor-associated neovascularization and is deregulated in many cancers. Unlike canonical cadherins, it lacks transmembrane and intracellular domains and is attached to the plasma membrane via a glycosylphosphatidylinositol anchor. T-cadherin is thought to function in signaling rather than as an adhesion molecule. Some interactive partners of T-cadherin at the plasma membrane have recently been identified. We examined T-cadherin location in human endothelial cells using confocal microscopy and subcellular fractionation. We found that a considerable proportion of T-cadherin is located in the nucleus and in the centrosomes. T-cadherin colocalized with a centrosomal marker -tubulin uniformly throughout the cell cycle at least in human umbilical vein endothelial cells. In the telophase, T-cadherin transiently concentrated in the midbody and was apparently degraded. Its overexpression resulted in an increase in the number of multinuclear cells, whereas its downregulation by small interfering RNA led to an increase in the number of cells with multiple centrosomes. These findings indicate that deregulation of T-cadherin in endothelial cells may lead to disturbances in cytokinesis or centrosomal replication.

cadherin family; cell cycle; cytokinesis; glycosylphosphatidylinositol anchor; human pulmonary artery endothelial cells