An article published this year in the
“Cellular
and Molecular Life Sciences” using one of our Specialized Antibody
Services, “Conjugation
Service”, by our customers from different centers in Spain and France , in
the analysis of Human endoglin as a potential new partner involved in
platelet–endothelium interactions. Congrats and Thanks.
Summay:
Complex
interactions between platelets and activated endothelium occur during the
thrombo-inflammatory reaction at sites of vascular injuries and during vascular
hemostasis. The endothelial receptor endoglin is involved in inflammation
through integrin-mediated leukocyte adhesion and transmigration; and
heterozygous mutations in the endoglin gene cause hereditary hemorrhagic
telangiectasia type 1. This vascular disease is characterized by a bleeding
tendency that is postulated to be a consequence of telangiectasia fragility
rather than a platelet defect, since platelets display normal functions in
vitro in this condition. Here, we hypothesize that endoglin may act as an
adhesion molecule involved in the interaction between endothelial cells and
platelets through integrin recognition. We find that the extracellular domain
of human endoglin promotes specific platelet adhesion under static conditions
and confers resistance of adherent platelets to detachment upon exposure to
flow. Also, platelets adhere to confluent endothelial cells in an
endoglin-mediated process. Remarkably, Chinese hamster ovary cells ectopically
expressing the human αIIbβ3 integrin
acquire the capacity to adhere to myoblast transfectants expressing human
endoglin, whereas platelets from Glanzmann’s thrombasthenia patients lacking
the αIIbβ3 integrin are
defective for endoglin-dependent adhesion to endothelial cells. Furthermore,
the bleeding time, but not the prothrombin time, is significantly prolonged in
endoglin-haplodeficient (Eng+/−) mice compared to Eng+/+ animals. These results suggest a new role for endoglin in αIIbβ3
integrin-mediated adhesion of platelets to the endothelium, and may provide a
better understanding on the basic cellular mechanisms involved in hemostasis
and thrombo-inflammatory events.
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