Biomedical Engineering Reference
In-Depth Information
Table 9.23. Extravasation-involved adhesion molecules (Source: [ 986 ] BM: basement mem-
brane; ICAM: intercellular adhesion molecule;). E-, L-, and P-selectins stand for endothelium,
lymphocyte, and platelet selectin, respectively. Sialomucins are secreted or membrane-associated
mucins that either act as adhesion receptors or anti-adhesive agent. Sialomucin core protein-24,
also called endolyn, multiglycosylated core protein MGC24, and CD164, is a cell adhesion
molecule. Selectin-P ligand (SelPLg; a.k.a. P-selectin glycoprotein ligand PSGL1 or CD162) is
a high-affinity receptor on myeloid cells and stimulated T lymphocytes for P-selectin on activated
platelets or endothelial cells. It can tether to E- and L-selectins with lower affinity.
Extravasation step
Adhesion molecules
Capture
Sialomucin, L-selectin, selectin-P ligand,
tethering
Integrin-
α 4 (leukocyte),
and rolling
E- and P-selectins, ICAM (endothelium)
Activation
Chemoattractants and GPCRs
Tight binding
Integrin-
β
2 and -
α
4 (leukocyte),
arrest
L-selectin, ICAM (endothelium)
Endothelium crossing
Cadherin-5
BM crossing
Integrin- β 1 and - β 2 ,
Migration in matrix
ICAM
Leukocytes are the largest flowing cells that must strongly deform to travel
into small blood vessels and traverse biological media. Leukocytes change their
shape permanently during migration. Once attached to the endothelium, they cross
tiny gaps between endothelial cells or even cross endothelial cells. Leukocyte
distribution in small vessel lumen depends on the interaction with the surrounding
erythrocytes susceptible to aggregation [ 976 , 977 ].
9.7.1
Flowing Cell Adhesion to Endothelium
Flowing cell adhesion to the endothelium starts with the penetration of the
glycocalyx, mainly at the endothelium of postcapillary venules, where endothelial
cells have weak tight junctions [ 978 ]. Circulating blood cells have adhesion
receptors that enable the cells subjected to flow forces to adhere to the vessel wall
(Table 9.23 ).
Between-cell interactions are initially reversible. Once tethered to the wall, a
cell forms an irreversible adhesion. Following adhesion to the blood vessel wall,
leukocytes change from an approximately spherical to a flattened shape due to a
reorganization of the actin cytoskeleton and polarization. Cell polarization with
a protrusive leading edge and a contractile rear is associated with a redistribu-
tion of intracellular signaling proteins and plasmalemmal receptors and adhesion
molecules.
 
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