This affects cell signaling, platelet and leukocyte adhesion to subendothelial matrix, vascular smooth muscle proliferation, inflammation, immune response, thrombosis, angiogenesis and angiocrine activities, and tumor niche formation leading to enhanced tumor implantation on endothelial surfaces [4, 47 55].
Upon injury they become exposed to subendothelial matrix proteins, particularly collagens, to which they initially adhere via the GPIb-V-IX complasmand plasma von Willebrand factor (VWF).
Activated platelets aggregate with circulating leukocytes and adhere to the subendothelial matrix and intact endothelium to mediate and recruit leukocytes into the vascular wall [ 11, 45, 46].
In addition, activated αvβ3 regulates protease maturation, is required for breast tumor cell interaction with platelets [ 5, 14, 31] and contributes to breast tumor cell adhesion to the subendothelial matrix under dynamic blood flow conditions [ 32].
In normal liver, vitronectin was restricted to the stroma of portal tracts and to the subendothelial matrix of central veins.
These data drive us to speculate that GD3 might act as second messenger in the activatory cascade, which leads to CD32 expression and triggers platelet adhesion and spreading to the subendothelial matrix.
Interestingly, EIB202 genome encodes a protein carrying homology to von Willebrand factor type A domain of humans (ETAE_3520, vwA), which is involved in the normal hemostasis by adhering to the subendothelial matrix following vascular damage [41].
Interestingly, these reactions occur on the surface of platelets that are anchored to the subendothelial matrix via collagen and vWF, which themselves activate the platelets along with the newly generated thrombin.
Clearly, neutrophils adhered to the subendothelial matrix and their adherence coincided with an increase in the percentage of exposed subendothelial matrix by the gradual contraction of endothelial cells.
A pool of neutrophil-derived myeloperoxidase is transcytosed and bound to the subendothelial matrix.
