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 d monocyte-derived dendritic cells within PA subendothelial and adventitial regions, influencing vasc

9 croscopy with the presence of characteristic subendothelial and mesangial curved, comma-like, banded

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

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

12 r H (CFH) and to promote the removal of both subendothelial and subepithelial immune complex (IC) dep

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

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

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

16 bridoma) caused IC deposition limited to the subendothelial area associated with unaltered CFH expres

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

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

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

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

21 IX (FIX) binds to collagen IV (Col4) in the subendothelial basement membrane.

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

23 junctions, thereby increasing sensitivity to subendothelial CCL5.

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

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

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

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

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

29 Exposed subendothelial collagen acts as a substrate for platelet

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

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

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

33 unfurl to release linear polymers that bind subendothelial collagen at wound sites, recruit platelet

34 vivo detection of tumor vasculature through subendothelial collagen binding.

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

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

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

38 in Ib-alpha, VWF-cleaving protease ADAMTS13, subendothelial collagen, and integrin alpha-IIb/beta-3.

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

40 articularly after phagocytosing particles in subendothelial collagen.

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

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

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

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

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

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

47 odocyte foot processes and subepithelial and subendothelial deposition.

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

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

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

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

52 NA in slowing the formation of mesangial and subendothelial electron-dense deposits.

53 largement (GECE) > 50% was present in 29.1%, subendothelial expansion/basement membrane duplication i

54 In multivariate analysis including DSA, subendothelial expansion/basement membrane duplication,

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

56 han that of arterial thrombosis initiated by subendothelial exposure.

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

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

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

60 microscopy experiments demonstrated stiffer subendothelial extracellular matrix in progeroid aortae,

61 barrier element, vascular flow factors, and subendothelial extracellular matrix mechanical propertie

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

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

64 Vessel wall subendothelial extracellular matrix, a dense mesh formed

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

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

67 A central collagen-rich subendothelial fibrillar layer (FL) correlates with area

68 and three-dimensional (3D) reconstruction of subendothelial foam cells provide visual evidence of lip

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

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

71 pression (1.7-fold) accompanied by decreased subendothelial IC deposition, as compared with NEP25/hyb

72 le of podocyte complement regulation in only subendothelial IC deposition.

73 uced CFH expression locally and clearance of subendothelial IC deposits.

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

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

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

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

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

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

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

81 valve endothelium and penetrated through the subendothelial layer.

82 uscle cells was primarily in the superficial subendothelial layer.

83 , which function to recruit monocytes to the subendothelial layer.

84 aggregation and to recruit platelets to the subendothelial layer.

85 nd aberrant activation of macrophages in the subendothelial layers govern atherosclerotic plaque deve

86 cumulation of lipid-laden macrophages in the subendothelial layers of affected blood vessels.

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

88 re positive for IgM and iC3b/c/d, indicating subendothelial leakage of plasma proteins.

89 assume a synthetic phenotype in response to subendothelial leakage of plasma proteins.

90 xtracellular matrix interactions, exposed in subendothelial lesions.

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

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

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

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

95 nterplay between endothelial dysfunction and subendothelial lipoprotein retention.

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

97 nteraction of arterial wall macrophages with subendothelial lipoproteins.

98 nesis is the interaction of macrophages with subendothelial lipoproteins.

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

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

101 et marginalization and both perivascular and subendothelial macrophage infiltration.

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

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

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

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

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

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

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

109 Monocytes that remained in the subendothelial matrix became macrophages.

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

111 itive erythrocytes adhere to endothelium and subendothelial matrix components.

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

113 endothelial cells (ECs) in plasma and in the subendothelial matrix has been shown to regulate angioge

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

129 uced retinal endothelial cell activation and subendothelial matrix remodeling.

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

131 in the form of lysyl oxidase (LOX)-dependent subendothelial matrix stiffening also contribute signifi

132 We also show that LOX-dependent subendothelial matrix stiffening feeds back to enhance r

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

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

135 ry, platelets adhere and spread over exposed subendothelial matrix substrates of the damaged blood ve

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

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

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

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

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

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

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

143 GPVI is activated by collagen in the subendothelial matrix, by fibrin and fibrinogen in the t

144 On subendothelial matrix, endogenous vWF and adsorbed plasm

145 Subendothelial matrix, fibronectin, or collagen I stimul

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

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

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

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

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

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

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

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

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

155 the retention of plasma lipoproteins in the subendothelial matrix.

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

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

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

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

160 is unable to interact with components of the subendothelial matrix.

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

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

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

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

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

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

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

168 it allows circulating lipoproteins to access subendothelial monocytes.

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

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

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

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

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

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

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

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

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

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

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

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

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

182 If the subendothelial retention of LDL by proteoglycans is the

183 The subendothelial retention of LDLs through their interacti

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

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

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

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

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

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

190 d, in vulnerable regions, is retained in the subendothelial space by binding to proteoglycans via spe

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

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

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

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

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

196 glycans (HSPGs)(2) and become trapped in the subendothelial space of large and medium size arteries,

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

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

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

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

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

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

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

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

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

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

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

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

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

210 ither lipid or monocytic infiltration of the subendothelial space.

211 ized to transmigrating pseudopods within the subendothelial space.

212 with diapedesis and migration in the narrow subendothelial space.

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

214 s, binds lipoprotein lipase (LPL) within the subendothelial spaces and shuttles it to the capillary l

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

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

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

218 , and accumulation of flocculent material in subendothelial spaces.

219 Endothelial cells respond to changes in subendothelial stiffness by altering their migration and

220 Both cell types respond to changes in subendothelial stiffness by increasing the traction stre

221 ovide insights into the relationship between subendothelial stiffness, endothelial mechanics and vari

222 othelial cell transcriptome, and reveal that subendothelial stiffness, while critically altering endo

223 -induced endothelial damage with exposure of subendothelial substrates.

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

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

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

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

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

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