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MBC in Press, published online ahead of print August 12, 2009
Mol. Biol. Cell 10.1091/mbc.E08-02-0210

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Submitted on February 26, 2008
Revised on July 6, 2009
Accepted on July 30, 2009

Golgi-associated cPLA2{alpha} Regulates Endothelial Cell-Cell Junction Integrity by Controlling the Trafficking of Transmembrane Junction Proteins

Elsa Regan-Klapisz,*{dagger} Vincent Krouwer,* Miriam Langelaar-Makkinje,* Laxman Nallan,{ddagger} Michael Gelb,{ddagger} Hans Gerritsen,{dagger} Arie J. Verkleij,* and Jan Andries Post*

*Cellular Architecture and Dynamics, Institute of Biomembranes, Utrecht University, 3584 CH Utrecht, The Netherlands; {dagger}Molecular Biophysics, Debye Institute for Nanomaterials Science, 3584 CC Utrecht, The Netherlands; {ddagger}Departments of Chemistry and Biochemistry, University of Washington, Seattle, WA 98195

Monitoring Editor: Vivek Malhotra

In endothelial cells specifically, cPLA2{alpha} translocates from the cytoplasm to the Golgi complex in response to cell confluence. Considering the link between confluence and cell-cell junction formation, and the emerging role of cPLA2{alpha} in intracellular trafficking, we tested whether Golgi-associated cPLA2{alpha} is involved in the trafficking of junction proteins. Here, we show that the redistribution of cPLA2{alpha} from the cytoplasm to the Golgi correlates with adherens junction maturation and occurs before tight junction formation. Disruption of adherens junctions using a blocking anti-VE-cadherin antibody reverses the association of cPLA2{alpha} with the Golgi. Silencing of cPLA2{alpha} and inhibition of cPLA2{alpha} enzymatic activity using various inhibitors result in the diminished presence of the transmembrane junction proteins VE-cadherin, occludin and claudin-5 at cell-cell contacts, and in their accumulation at the Golgi. Altogether, our data support the idea that VE-cadherin triggers the relocation of cPLA2{alpha} to the Golgi, and that in turn, Golgi-associated cPLA2{alpha} regulates the transport of transmembrane junction proteins through or from the Golgi, thereby controlling the integrity of endothelial cell-cell junctions.

Address correspondence to: Elsa Regan-Klapisz (E.E.Regan1{at}uu.nl)






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