TY - JOUR
T1 - VIGR - A novel inducible adhesion family G-protein coupled receptor in endothelial cells
AU - Stehlik, Christian
AU - Kroismayr, Renate
AU - Dorfleutner, Andrea
AU - Binder, Bernd R.
AU - Lipp, Joachim
N1 - Funding Information:
We gratefully acknowledge David Blanco for providing plasmid pMG, Margarethe Geiger and Zydi Zhegu for immunization of rabbits and isolation of HSMECs and HUVEC, and Renate Hofer-Warbinek for providing the HM2, HM39/2, HM60, and HU2 cell lines. This work was supported by Biomolecular Therapeutics GmbH and a grant to J.L. from the Jubilaeumsfonds of the Austrian National Bank, Project 8114.
PY - 2004/7/2
Y1 - 2004/7/2
N2 - Using a signal sequence trap for selection of differentially expressed secretory and membrane proteins, we identified a novel member of the adhesion family of G-protein coupled receptors (GPCRs), termed vascular inducible GPCR (VIGR). VIGR contains C1r-C1s, Uegf and Bmp1 (CUB) and pentraxin (PTX)-like modules and a mucin-like spacer, followed by seven transmembrane domains. By surface biotinylation as well as by immunofluorescence analysis we demonstrate that endogenous, highly glycosylated VIGR is expressed on the cell surface of endothelial cells (ECs) upon LPS or thrombin treatment, and inducible expression is mediated by MAP kinases, but not NF-κB. We show that VIGR is selectively expressed in ECs derived from larger vessels, but not from microvessels. In summary, VIGR represents a novel GPCR of the adhesion family, which is unique in its long extra-cellular domain comprising CUB and PTX-like modules and in its inducibility by LPS and thrombin in a subset of ECs, suggesting an important function in cell-adhesion and potentially links inflammation and coagulation.
AB - Using a signal sequence trap for selection of differentially expressed secretory and membrane proteins, we identified a novel member of the adhesion family of G-protein coupled receptors (GPCRs), termed vascular inducible GPCR (VIGR). VIGR contains C1r-C1s, Uegf and Bmp1 (CUB) and pentraxin (PTX)-like modules and a mucin-like spacer, followed by seven transmembrane domains. By surface biotinylation as well as by immunofluorescence analysis we demonstrate that endogenous, highly glycosylated VIGR is expressed on the cell surface of endothelial cells (ECs) upon LPS or thrombin treatment, and inducible expression is mediated by MAP kinases, but not NF-κB. We show that VIGR is selectively expressed in ECs derived from larger vessels, but not from microvessels. In summary, VIGR represents a novel GPCR of the adhesion family, which is unique in its long extra-cellular domain comprising CUB and PTX-like modules and in its inducibility by LPS and thrombin in a subset of ECs, suggesting an important function in cell-adhesion and potentially links inflammation and coagulation.
KW - CUB, C1r-C1s, Uegf and Bmp1
KW - EC, endothelial cell
KW - GPCR, G-protein coupled receptor
KW - GPS, GPCR proteolytic site
KW - HAECs, human aortic ECs
KW - HSMECs, human skin microvascular ECs
KW - HUVECs, human umbilical vein ECs
KW - LPS, lipopolysaccharide
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U2 - 10.1016/j.febslet.2004.05.038
DO - 10.1016/j.febslet.2004.05.038
M3 - Article
C2 - 15225624
AN - SCOPUS:3042553740
SN - 0014-5793
VL - 569
SP - 149
EP - 155
JO - FEBS Letters
JF - FEBS Letters
IS - 1-3
ER -