Abstract:
:HLA-G is a major histocompatibility complex class Ib molecule whose constitutive tissue distribution is restricted mainly to trophoblast cells at the maternal-fetal interface during pregnancy. In this study, we demonstrated the ability of the soluble HLA-G1 (sHLA-G1) isoform to inhibit fibroblast growth factor-2 (FGF2)-induced capillary-like tubule formation. Using a rabbit corneal neovascularization model, we further showed that sHLA-G1 inhibits FGF2-induced angiogenesis in vivo. We also demonstrated that sHLA-G1 induces endothelial cell apoptosis through binding to BY55/CD160, a glycosylphosphatidylinositolanchored receptor expressed by endothelial cells. Furthermore, we showed that the specific CL1-R2 anti-CD160 monoclonal antibody mimics sHLA-G1-mediated inhibition of endothelial cell tube formation and induction of apoptosis. Thus, the engagement of CD160 in endothelial cells may be essential for the inhibition of angiogenesis. sHLA-G1/CD160-mediated antiangiogenic property may participate in the vascular remodeling of maternal spiral arteries during pregnancy, and, given that we found that CD160 is strongly expressed in the vasculature of a murine tumor, it offers an attractive therapeutic target for preventing pathologic neovascularization.
journal_name
Bloodjournal_title
Bloodauthors
Fons P,Chabot S,Cartwright JE,Lenfant F,L'Faqihi F,Giustiniani J,Herault JP,Gueguen G,Bono F,Savi P,Aguerre-Girr M,Fournel S,Malecaze F,Bensussan A,Plouët J,Le Bouteiller Pdoi
10.1182/blood-2005-12-019919subject
Has Abstractpub_date
2006-10-15 00:00:00pages
2608-15issue
8eissn
0006-4971issn
1528-0020pii
blood-2005-12-019919journal_volume
108pub_type
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