Chemistry Reference
In-Depth Information
Figure 29.5
(a) Adhesion molecules involved in
platelet rolling along the activated endothelium.
The endothelial ligand-mediating rolling of acti-
vated platelets is unknown. (b) Platelet-medi-
ated leukocyte recruitment at sites of vascular
damage. Adhesion of leukocytes to activated
platelets is mediated by P-selectin. Firm adhe-
sion and emigration of leukocytes to the site of
infl ammation is mediated by
β
2
integrins (not
shown). (c) Platelet-mediated tumor cell recruit-
ment at sites of vascular damage. Platelets acti-
vated at sites of vascular damage mediate tumor
cell recruitment through P - selectin - dependent
tethering and rolling, and
β
3
integrin - dependent
adhesion.
angiogenesis, specifi cally during tumor growth [16]. Platelets activated at the site
of vascular damage mediate tumor cell recruitment through P-selectin-tumor cell
tethering and rolling followed by stable adhesion mediated by
3
and VWF
(Figure 29.5). Some investigators have suggested that a specifi c tumor cell/endo-
thelium/platelet interaction may contribute to tumor- induced angiogenesis, since
activated platelets release vascular endothelial growth factor - a potent proangio-
genic factor. Interestingly, pro- and antiangiogenic proteins are organized into
separate platelet
α
IIb
β
-granules and differentially released. It is possible that dense
granules containing Golgi enzymes and donor substrates are well organized and
differentially released following platelet activation.
α
29.6
Conclusions
After vessel wall injury, platelets tether and roll on exposed subendothelial tissues
through the interaction between the GPIb
subunit of their GPIb-IX-V receptor
and collagen-bound VWF. Unlike leukocyte rolling mediated by selectins, GPIb
α
-
dependent platelet rolling on VWF has never been reported to be glycan depen-
α
