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1 is unable to interact with components of the subendothelial matrix.
2 were present as a maturation stimulus in the subendothelial matrix.
3 heparan sulfate, laminin, or collagen in the subendothelial matrix.
4  the retention of plasma lipoproteins in the subendothelial matrix.
5 nt of highly sulfated heparin-like HS in the subendothelial matrix.
6 ding of LDL to artery derived decorin and to subendothelial matrix.
7 its adhesion to endothelial cells and to the subendothelial matrix.
8 ce of TN on the surface of HBMECs and in the subendothelial matrix.
9 Although the biology of platelet adhesion on subendothelial matrix after vascular injury is well char
10            This enhances deposition of Fg in subendothelial matrix and interstitium making the immobi
11   Binding of lipoprotein (a) [Lp(a)] to both subendothelial matrix and Matrigel(R) increased 2-10-fol
12 oB100- containing lipoproteins with heparin, subendothelial matrix, and artery wall purified proteogl
13 ha2(VIII) collagen, a major component of the subendothelial matrix, and examined the ability of and m
14 ver, RBC interactions with components of the subendothelial matrix are not well-characterized.
15        Rather than penetrate deeply into the subendothelial matrix, as is seen with untreated control
16               Monocytes that remained in the subendothelial matrix became macrophages.
17          Most migrated cells remained in the subendothelial matrix, but ~10% underwent spontaneous ba
18 a containing apoB17 decreased LDL binding to subendothelial matrix by 42%.
19         GPVI is activated by collagen in the subendothelial matrix, by fibrin and fibrinogen in the t
20 itive erythrocytes adhere to endothelium and subendothelial matrix components.
21                                           On subendothelial matrix, endogenous vWF and adsorbed plasm
22                                              Subendothelial matrix, fibronectin, or collagen I stimul
23 cal step in the adhesion of platelets to the subendothelial matrix following endothelial cell damage,
24 young thrombocytes, they adhere first to the subendothelial matrix, get activated rapidly, release ag
25 endothelial cells (ECs) in plasma and in the subendothelial matrix has been shown to regulate angioge
26 tribute to erythrocyte interactions with the subendothelial matrix, hereby participating in the patho
27                                  However, in subendothelial matrix in blood vessels and in the baseme
28  the ability to sustain protrusions into the subendothelial matrix in contrast with control cells.
29 telets rapidly adhere to the site of exposed subendothelial matrix in the vessel wall, become activat
30              Platelet microparticles bind to subendothelial matrix in vitro and in vivo and can act a
31 cells (RBCs) to the vascular endothelium and subendothelial matrix likely plays a significant role in
32 vascular HS(act) predominantly occurs in the subendothelial matrix, mice were subjected to a carotid
33 lipoprotein B lipoproteins with the specific subendothelial matrix molecules that mediate retention a
34 at mediates the adhesion of platelets to the subendothelial matrix of injured blood vessels.
35 turns to baseline; the basement membrane and subendothelial matrix of the inner wall appear to remain
36 urned to baseline; the basement membrane and subendothelial matrix of the inner wall remained intact.
37 e incorporated dying autologous cells in the subendothelial matrix of the model.
38 Herein, we show that MPO concentrates in the subendothelial matrix of vascular tissues by a transcyto
39  ligand, von Willebrand factor (vWF), in the subendothelial matrix or plasma.
40                      On interaction with the subendothelial matrix, platelets are transformed into ba
41 Cs) have enhanced adhesion to the plasma and subendothelial matrix protein thrombospondin-1 (TSP) und
42 ere to HUVECs, whereas only spores adhere to subendothelial matrix proteins.
43 epositing them to collagen and other exposed subendothelial matrix proteins.
44 uced retinal endothelial cell activation and subendothelial matrix remodeling.
45                  Inhibition of LOX-dependent subendothelial matrix stiffening alone suppressed HG-ind
46 in the form of lysyl oxidase (LOX)-dependent subendothelial matrix stiffening also contribute signifi
47              We also show that LOX-dependent subendothelial matrix stiffening feeds back to enhance r
48 s of tunable stiffness, we demonstrated that subendothelial matrix stiffening is necessary and suffic
49 that HG significantly enhances LOX-dependent subendothelial matrix stiffness in vitro, which correlat
50 ry, platelets adhere and spread over exposed subendothelial matrix substrates of the damaged blood ve
51 lymorphonuclear leukocytes [PMNs]) encounter subendothelial matrix substrates that may require additi
52 IIb/IIIa) to interact with components of the subendothelial matrix, such as fibronectin (Fn), exposed
53      Platelets interact with collagen in the subendothelial matrix that is exposed by vascular damage
54 elets initially adhere on vWF affixed to the subendothelial matrix through the glycoprotein (GP) Ib-I
55 W) VWF is targeted basolaterally, toward the subendothelial matrix, using the adaptor protein complex
56                                 To mimic the subendothelial matrix, vWF was microarrayed over sonicat