ライフサイエンスコーパス: subendothelial

1 l disease process characterized by the focal subendothelial accumulation of apolipoprotein-B-containi

2 erial 16s ribosomal DNA as well as increased subendothelial accumulation of CD68(+) monocytes/macroph

3 inflammatory vascular disease driven by the subendothelial accumulation of macrophages.

4 ity by causing monocyte subset imbalance and subendothelial accumulation, raising a note of caution r

5 lerosis, a chronic inflammatory disease with subendothelial accumulation; (iii) the TLR4 is not only

6 The subendothelial aggregation and retention of low density

7 Thickened chordae showed endothelial and subendothelial alpha-smooth muscle actin.

8 ition along the portal stroma, central vein, subendothelial and stromal space in the patients with pe

9 Collagen VIII is localized in subendothelial and subepithelial extracellular matrices.

10 Ultrastructurally, there were subendothelial and subepithelial immune deposits and ext

11 which by electron microscopy were present in subendothelial and subepithelial immune deposits, wherea

12 stributed broadly within the endothelial and subendothelial aortic layers, in contrast to mature defi

13 ountered on endothelial surface (apical) and subendothelial (basal) compartments.

14 l capillary endothelial cells (ECs) enhances subendothelial basement membrane (BM) stiffness, which,

15 ing TEM, neutrophils must still traverse the subendothelial basement membrane and network of pericyte

16 CatS(-/-)LDLR(-/-) monocytes showed impaired subendothelial basement membrane transmigration, and aor

17 mark of humoral rejection is the presence of subendothelial C4d in the allograft.

18 junctions, thereby increasing sensitivity to subendothelial CCL5.

19 to undergo robust LFA-1-dependent TEM toward subendothelial CCL5.

20 s observed when vWf was a constituent of the subendothelial cell matrix and when it was bound to puri

21 l contraction and that this event depends on subendothelial cell matrix stiffness.

22 ructive arterial disease, which results from subendothelial cell proliferation and reorganization of

23 nd amplified chemotaxis to an otherwise weak subendothelial chemokine signal.

24 Exposed subendothelial collagen acts as a substrate for platelet

25 of the platelet alpha 2 beta 1 integrin with subendothelial collagen after vascular injury are requir

26 It does this by forming a bridge between subendothelial collagen and the platelet glycoprotein Ib

27 imaging tracer that specifically binds tumor subendothelial collagen and thereby images tumor vascula

28 vivo detection of tumor vasculature through subendothelial collagen binding.

29 hic imaging allows identification of exposed subendothelial collagen in injured WT and high-fat diet-

30 lets will enable them to bind injury-exposed subendothelial collagen to initiate platelet activation.

31 multimers and binds poorly to platelets and subendothelial collagen upon LVAD implantation, leading

32 Plaque erosion leads to exposure of subendothelial collagen, which may be targeted by glycop

33 articularly after phagocytosing particles in subendothelial collagen.

34 t has binding sites for platelets as well as subendothelial collagen.

35 Under normal conditions, subendothelial collagens bear the GPVI-binding sites tha

36 l cells (HUVECs) when displayed alone in the subendothelial compartment under static or hemodynamic s

37 uent recovery of HIV-infected cells from the subendothelial compartment.

38 eleased from activated platelets adherent to subendothelial connective tissue is a principal smooth m

39 hanges were seen in mutants, including focal subendothelial delamination and widespread podocyte foot

40 odocyte foot processes and subepithelial and subendothelial deposition.

41 minal pathway, and the highest prevalence of subendothelial deposits, but those in cluster 2 had addi

42 ic-type cells that reverse-migrated from the subendothelial depot to the apical endothelial surface 4

43 nectin and fibrinogen are deposited into the subendothelial ECM at atherosclerosis-prone sites at ear

44 ted with endothelial disruption, exposure of subendothelial ECM could induce complement fixation and

45 lief, FeCl(3) does not result in appreciable subendothelial exposure within the time frame of thrombo

46 han that of arterial thrombosis initiated by subendothelial exposure.

47 elial cell integrins, which then bind to the subendothelial extracellular matrix (ECM), and, in cells

48 ntrated not on cells but in areas of exposed subendothelial extracellular matrix (ECM).

49 ns, resulting in new integrin binding to the subendothelial extracellular matrix and signaling.

50 ential accumulation of SIP(F8)-SS-DM1 in the subendothelial extracellular matrix of tumors, similar t

51 We propose that glycosaminoglycans in the subendothelial extracellular matrix serve to augment the

52 Vessel wall subendothelial extracellular matrix, a dense mesh formed

53 ounter lipoproteins that are mostly bound to subendothelial extracellular matrix, and these lipoprote

54 s highly dependent on the composition of the subendothelial extracellular matrix.

55 ranase may play a critical role in releasing subendothelial HS bound proteins, and specific HS oligos

56 Vascular changes included progressive subendothelial hyalinization, with luminal narrowing or

57 n 26-week allografts, we found mesangial and subendothelial immune complex-type electron-dense deposi

58 matrix and accumulation of immune-deposits, subendothelial immune-deposits, focal occlusion of capil

59 en infected apoE(-/-) mice had a significant subendothelial infiltrate composed of a heterogeneous gr

60 Focal endothelial proliferation and subendothelial inflammatory cells were found in sections

61 adhesion via alpha3beta1 and alpha6beta1 to subendothelial laminin was a critical prerequisite for s

62 cells deposit CD18(+) microparticles at the subendothelial layer before retracting the stretched uro

63 lving inflammatory response that expands the subendothelial layer due to the accumulation of cells, l

64 valve endothelium and penetrated through the subendothelial layer.

65 aggregation and to recruit platelets to the subendothelial layer.

66 uscle cells was primarily in the superficial subendothelial layer.

67 wall SMase that hydrolyzes LDL-SM and causes subendothelial LDL aggregation.

68 to binding to exposed type I collagen in the subendothelial lining of damaged blood vessels, facilita

69 A quantitative assessment of subendothelial lipid deposition by freeze-fracture and d

70 ct the distribution or amount of aortic arch subendothelial lipid deposits.

71 and in vivo data have implicated S-SMase in subendothelial lipoprotein aggregation, macrophage foam

72 nterplay between endothelial dysfunction and subendothelial lipoprotein retention.

73 nteraction of arterial wall macrophages with subendothelial lipoproteins have demonstrated an initial

74 nteraction of arterial wall macrophages with subendothelial lipoproteins.

75 nesis is the interaction of macrophages with subendothelial lipoproteins.

76 x vivo confocal microscopy confirmed LO1-750 subendothelial localization of LO1-750 at sites of ather

77 and ultrastructural lesions (mesangiolysis, subendothelial lucency, platelet thrombi in glomerular c

78 ism by which platelets interact with exposed subendothelial matrices following vascular injury.

79 telet aggregates and potentiates adhesion to subendothelial matrices via fibrin(ogen), von Willebrand

80 e RBC to vascular endothelial cells (EC) and subendothelial matrices.

81 Although the biology of platelet adhesion on subendothelial matrix after vascular injury is well char

82 This enhances deposition of Fg in subendothelial matrix and interstitium making the immobi

83 Binding of lipoprotein (a) [Lp(a)] to both subendothelial matrix and Matrigel(R) increased 2-10-fol

84 ver, RBC interactions with components of the subendothelial matrix are not well-characterized.

85 Monocytes that remained in the subendothelial matrix became macrophages.

86 a containing apoB17 decreased LDL binding to subendothelial matrix by 42%.

87 itive erythrocytes adhere to endothelium and subendothelial matrix components.

88 cal step in the adhesion of platelets to the subendothelial matrix following endothelial cell damage,

89 However, in subendothelial matrix in blood vessels and in the baseme

90 the ability to sustain protrusions into the subendothelial matrix in contrast with control cells.

91 telets rapidly adhere to the site of exposed subendothelial matrix in the vessel wall, become activat

92 Platelet microparticles bind to subendothelial matrix in vitro and in vivo and can act a

93 cells (RBCs) to the vascular endothelium and subendothelial matrix likely plays a significant role in

94 lipoprotein B lipoproteins with the specific subendothelial matrix molecules that mediate retention a

95 at mediates the adhesion of platelets to the subendothelial matrix of injured blood vessels.

96 turns to baseline; the basement membrane and subendothelial matrix of the inner wall appear to remain

97 urned to baseline; the basement membrane and subendothelial matrix of the inner wall remained intact.

98 e incorporated dying autologous cells in the subendothelial matrix of the model.

99 Herein, we show that MPO concentrates in the subendothelial matrix of vascular tissues by a transcyto

100 ligand, von Willebrand factor (vWF), in the subendothelial matrix or plasma.

101 Cs) have enhanced adhesion to the plasma and subendothelial matrix protein thrombospondin-1 (TSP) und

102 epositing them to collagen and other exposed subendothelial matrix proteins.

103 ere to HUVECs, whereas only spores adhere to subendothelial matrix proteins.

104 Inhibition of LOX-dependent subendothelial matrix stiffening alone suppressed HG-ind

105 s of tunable stiffness, we demonstrated that subendothelial matrix stiffening is necessary and suffic

106 that HG significantly enhances LOX-dependent subendothelial matrix stiffness in vitro, which correlat

107 lymorphonuclear leukocytes [PMNs]) encounter subendothelial matrix substrates that may require additi

108 Platelets interact with collagen in the subendothelial matrix that is exposed by vascular damage

109 elets initially adhere on vWF affixed to the subendothelial matrix through the glycoprotein (GP) Ib-I

110 oB100- containing lipoproteins with heparin, subendothelial matrix, and artery wall purified proteogl

111 ha2(VIII) collagen, a major component of the subendothelial matrix, and examined the ability of and m

112 Rather than penetrate deeply into the subendothelial matrix, as is seen with untreated control

113 Most migrated cells remained in the subendothelial matrix, but ~10% underwent spontaneous ba

114 On subendothelial matrix, endogenous vWF and adsorbed plasm

115 Subendothelial matrix, fibronectin, or collagen I stimul

116 young thrombocytes, they adhere first to the subendothelial matrix, get activated rapidly, release ag

117 tribute to erythrocyte interactions with the subendothelial matrix, hereby participating in the patho

118 vascular HS(act) predominantly occurs in the subendothelial matrix, mice were subjected to a carotid

119 On interaction with the subendothelial matrix, platelets are transformed into ba

120 IIb/IIIa) to interact with components of the subendothelial matrix, such as fibronectin (Fn), exposed

121 W) VWF is targeted basolaterally, toward the subendothelial matrix, using the adaptor protein complex

122 To mimic the subendothelial matrix, vWF was microarrayed over sonicat

123 its adhesion to endothelial cells and to the subendothelial matrix.

124 were present as a maturation stimulus in the subendothelial matrix.

125 heparan sulfate, laminin, or collagen in the subendothelial matrix.

126 the retention of plasma lipoproteins in the subendothelial matrix.

127 nt of highly sulfated heparin-like HS in the subendothelial matrix.

128 ding of LDL to artery derived decorin and to subendothelial matrix.

129 ce of TN on the surface of HBMECs and in the subendothelial matrix.

130 study was undertaken to investigate whether subendothelial mesenchymal cells may emerge through tran

131 nistically, inhibition of lymph node homing, subendothelial migration and cell polarization, but not

132 a gender difference in monocyte adhesion and subendothelial migration in hypercholesterolemic rabbits

133 e rabbits develop more monocyte adhesion and subendothelial migration than do female rabbits during h

134 Monocyte adhesion and subendothelial migration were assessed in a blinded fash

135 ester loading (foam cell formation), require subendothelial modification of the retained lipoproteins

136 pplementation demonstrate fewer adherent and subendothelial monocytes than do oophorectomized rabbits

137 it allows circulating lipoproteins to access subendothelial monocytes.

138 graft liver characterized by perivenular and subendothelial mononuclear inflammation of the terminal

139 onsistently increased in the endothelium and subendothelial neointimal regions of elastic pulmonary a

140 of the predisposition of LDL to the in vivo subendothelial oxidative stress.

141 ron-laden macrophages were present either in subendothelial plaque surfaces or in thin layers overlyi

142 as small "lakes" deeper in the artery, in a subendothelial position.

143 d exposure of circulating factor VII/VIIa to subendothelial procoagulants such as TF leads to intrava

144 Plaque disruption and exposure of subendothelial procoagulants such as tissue factor (TF)

145 Disruption of elastin is enough to induce subendothelial proliferation of smooth muscle and may co

146 o the endothelium and to exposed, underlying subendothelial proteins is believed to contribute to vas

147 both in endothelium overlying plaques and in subendothelial regions, providing multiple pathways for

148 S-SMase may cause subendothelial retention and aggregation of lipoproteins

149 y initiating process in atherogenesis is the subendothelial retention of apolipoprotein B-containing

150 iating event in early atherosclerosis is the subendothelial retention of cholesterol-rich, atherogeni

151 If the subendothelial retention of LDL by proteoglycans is the

152 The subendothelial retention of LDLs through their interacti

153 capacity of reverse transmigrating (RT) and subendothelial (SE) monocytes were compared.

154 rupt reductions in fluid shear stress induce subendothelial smooth muscle cells (SMCs) to proliferate

155 Atherosclerosis occurs in the subendothelial space (intima) of medium-sized arteries a

156 of disease, monocytes transmigrate into the subendothelial space and differentiate into foam cells.

157 erized proteolytic systems to infiltrate the subendothelial space and generate neointimal lesions.

158 es with senescence markers accumulate in the subendothelial space at the onset of atherosclerosis, wh

159 ed macrophage "foam cells" accumulate in the subendothelial space during the development of fatty str

160 Although lipid peroxidation in the subendothelial space has been hypothesized to play a cen

161 Oxidation of LDL in the subendothelial space has been proposed to play a key rol

162 Monocytes enter the subendothelial space in response to a variety of chemota

163 The release of cytokines in the subendothelial space may have a significant role in prom

164 t (transfer of macrophage-cholesterol in the subendothelial space of the arterial wall to the liver)

165 transports lipoprotein lipase (LPL) from the subendothelial space to the luminal side of the capillar

166 an is the major HSPG of mesangial matrix and subendothelial space, and consistent with this, blockade

167 Oxidized LDL has been found within the subendothelial space, and it exhibits numerous atherogen

168 thelial cells, stellate cells located in the subendothelial space, and liver parenchymal cells, take

169 microscopy studies showed C3 deposits in the subendothelial space, associated with unusual deposits l

170 is, circulating macrophages migrate into the subendothelial space, internalize cholesterol-rich lipop

171 cumulation of lipid-laden macrophages in the subendothelial space.

172 ity of the eosinophils being arrested in the subendothelial space.

173 ither lipid or monocytic infiltration of the subendothelial space.

174 ized to transmigrating pseudopods within the subendothelial space.

175 with diapedesis and migration in the narrow subendothelial space.

176 here to the endothelium and migrate into the subendothelial space.

177 on endothelium and leukocytes but not in the subendothelial space.

178 ates and accumulated in large amounts in the subendothelial space.

179 vascular smooth muscle cells (VSMC) into the subendothelial space.

180 an important means of delivering MPO to the subendothelial space.

181 transports lipoprotein lipase (LPL) from the subendothelial spaces to the capillary lumen.

182 ells, shuttles lipoprotein lipase (LPL) from subendothelial spaces to the capillary lumen.

183 lial cells and subsequently migrate into the subendothelial spaces, where they differentiate into mac

184 , and accumulation of flocculent material in subendothelial spaces.

185 -induced endothelial damage with exposure of subendothelial substrates.

186 th TF on ECs and leukocytes but less so with subendothelial TF.

187 et membrane glycoproteins mediate binding to subendothelial tissue and aggregation into haemostatic p

188 vs homing to atherosclerotic endothelial and subendothelial tissues, and lesion-associated biomarkers

189 initiates the adherence of platelets to the subendothelial vasculature under the high shear that occ

190 Ib (GPIb) surface receptor and its arterial subendothelial von Willebrand factor (vWF) ligand.

191 re it may provide the bulk of collagen-bound subendothelial VWF.