ライフサイエンスコーパス: VCAM-1

1 VCAM-1 and ICAM-1 were the endothelial adhesion molecule

2 VCAM-1 and osteopontin demonstrated sustained upregulati

3 VCAM-1 expression by cholangiocytes contributes to persi

4 VCAM-1 expression correlated with tumor stage.

5 VCAM-1 expression detected by MRI increased significantl

6 VCAM-1 peaked at 2 dynes/cm(2) and decreased to below st

7 VCAM-1 was detected on BDs in CLDs (primary biliary cirr

8 maging of vascular cell adhesion molecule-1 (VCAM 1) P-selectin, and platelet glycoprotein-1balpha (G

9 n ligands vascular cell adhesion molecule 1 (VCAM-1) and fibronectin, whereas inhibition of MEK/ERK b

10 f soluble vascular cell adhesion molecule 1 (VCAM-1) and osteoprotegerin were significantly associate

11 n between vascular cell adhesion molecule 1 (VCAM-1) and very late antigen-4 (VLA-4) played an integr

12 Vascular cell adhesion molecule 1 (VCAM-1) expression, however, was unaffected by the disea

13 AM-1) and vascular cell adhesion molecule 1 (VCAM-1) in the lungs of infected RIP2(-/-) mice were att

14 Vascular cell adhesion molecule 1 (VCAM-1) plays a major role in the chronic inflammatory p

15 inding to vascular cell adhesion molecule 1 (VCAM-1) upregulated on inflamed arterial endothelium.

16 l (HUVEC) vascular cell adhesion molecule 1 (VCAM-1) upregulation.

17 Levels of vascular cell adhesion molecule 1 (VCAM-1) were measured by sandwich enzyme-linked immunoso

18 red pulp vascular cell adhesion molecule 1 (VCAM-1)(+) macrophages are essential to extramedullary m

19 captures vascular cell adhesion molecule 1 (VCAM-1)(+) metastatic tumor cells, thereby promoting lym

20 targeting vascular cell adhesion molecule 1 (VCAM-1), a marker of atherosclerotic plaques, was constr

21 y marker, vascular cell adhesion molecule 1 (VCAM-1), in atherosclerotic plaques.

22 including vascular cell adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), E-s

23 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), platelet-endothelial cell adhesion molecule 1 (

24 or human vascular cell adhesion molecule 1 (VCAM-1), recently has been proposed as a new imaging age

25 (ICAM-1)/vascular cell adhesion molecule 1 (VCAM-1)-mediated adhesion of both macrophages and neutro

26 d a novel vascular cell adhesion molecule 1 (VCAM-1)-targeted magnetic resonance imaging (MRI) contra

27 ectin and vascular cell adhesion molecule 1 (VCAM-1).

28 AM-1) and vascular cell adhesion molecule 1 (VCAM-1).

29 Vascular cell adhesion molecule 1 (VCAM-1; CD106), a member of the immunoglobulin superfami

30 P = .02); vascular cell adhesion molecule-1 (VCAM-1) (Group I: 0.34 (0.67) ng/mL, Group II: 0.11 (0.1

31 ocytes to vascular cell adhesion molecule-1 (VCAM-1) activates signals in endothelial cells, includin

32 ession of vascular cell adhesion molecule-1 (VCAM-1) and could be mimicked by knockdown of mammalian

33 proteins vascular cell adhesion molecule-1 (VCAM-1) and endothelial nitric oxide synthase, whereas P

34 on of the vascular cell adhesion molecule-1 (VCAM-1) and monocyte adhesion to coronary artery endothe

35 sensitive vascular cell adhesion molecule-1 (VCAM-1) and monocyte chemotactic protein-1 (MCP-1) in is

36 n markers vascular cell adhesion molecule-1 (VCAM-1) and vascular adhesion protein-1 (VAP-1).

37 hMSCs and vascular cell adhesion molecule-1 (VCAM-1) blockade on HSECs.

38 AM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression by redox-dependent mechanisms that in

39 lation of vascular cell adhesion molecule-1 (VCAM-1) expression in a PKCepsilon- and NF-kappaB-depend

40 Vascular cell adhesion molecule-1 (VCAM-1) expression was notable in blood vessels, as was

41 ce global vascular cell adhesion molecule-1 (VCAM-1) expression.

42 ence that vascular cell adhesion molecule-1 (VCAM-1) imaging in atherosclerotic mice is feasible and

43 (TF) and vascular cell adhesion molecule-1 (VCAM-1) in diabetic apoE(-/-)hAR mice aortas and in high

44 ession of vascular cell adhesion molecule-1 (VCAM-1) in primary culture of tumour endothelial cells.

45 Vascular cell adhesion molecule-1 (VCAM-1) is expressed on the mesothelium of ovarian cance

46 Vascular cell adhesion molecule-1 (VCAM-1) plays important roles in development and inflamm

47 ), and soluble vascular adhesion molecule-1 (VCAM-1)) using baseline data from 668 participants (age,

48 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin, resulting in a decreased adhesi

49 (MCP-1), vascular cell adhesion molecule-1 (VCAM-1), nuclear factor kappaB (NF-kappaB), endothelial

50 le-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1), P-selectin, and L-selectin, function to facilit

51 dothelial vascular cell adhesion molecule-1 (VCAM-1), which is required for eosinophil accumulation.

52 inding to vascular cell adhesion molecule-1 (VCAM-1), which is upregulated in inflamed endothelial ce

53 ession of vascular cell adhesion molecule-1 (VCAM-1), which regulates leukocyte extravasation.

54 AM-1) and vascular cell adhesion molecule-1 (VCAM-1).

55 lesional vascular cell adhesion molecule-1 (VCAM-1).

56 diated by vascular cell adhesion molecule-1 (VCAM-1).

57 dothelial vascular cell adhesion molecule-1 (VCAM-1).

58 CAM-1) and vascular cell adhesion protein 1 (VCAM-1) under flow conditions.

59 iostin and vascular cell adhesion protein 1 (VCAM-1), molecules that mediate leukocyte infiltration a

60 olecules (vascular cell adhesion molecule 1 [VCAM-1] and intracellular adhesion molecule 1 [ICAM-1]).

61 es 1; and vascular cell adhesion molecule 1 [VCAM-1]) were measured by using enzyme-linked immunosorb

62 (4.4-folds); decreased expression of ICAM-1, VCAM-1 (3.2-fold), along with reduced levels of cytokine

63 F-beta, NFkappaB, MCP-1, IL-1, IL-6, ICAM-1, VCAM-1 and CD68 macrophages.

64 ory cytokine production (E-selectin, ICAM-1, VCAM-1 and IL-6).

65 The expression of ICAM-1, VCAM-1 and of MCP-1 was elevated and apoptosis was incre

66 hemokines and is mediated in part by ICAM-1, VCAM-1, and ALCAM.

67 e proinflammatory adhesion molecules ICAM-1, VCAM-1, and E-selectin, as well as the proinflammatory c

68 ung sections, and mRNA expression of ICAM-1, VCAM-1, E-selectin, RANTES, IL-17, IL-33, thymic stromal

69 lial, and/or vascular CAMs (ICAM-1, PECAM-1, VCAM-1).

70 1-targeted nanocarriers outperformed PECAM-1/VCAM-1 in control and disease-like conditions, and tripl

71 AM-1-targeted nanocarriers surpassed PECAM-1/VCAM-1 in control, but showed lower selectivity toward d

72 In endothelial cells, binding of PECAM-1/VCAM-1-targeted nanocarriers was intermediate to single-

73 rmed cells, and targeting NF-kappaB or VLA-4/VCAM-1 signaling could be a clinically relevant mechanis

74 High concentrations of MMP-7, ICAM-1, IL-8, VCAM-1, and S100A12 predicted poor overall survival, poo

75 We exemplified this strategy by generating a VCAM-1-targeted perfluorocarbon nanoparticle for in vivo

76 Recruitment from blood to a VCAM-1 substrate under shear stress was assessed ex vivo

77 inhibition of endothelial activation with a VCAM-1 blocking antibody or a VAP-1 small molecule inhib

78 ADAP, and Pyk2, the strength of alpha4beta1-VCAM-1 interaction and cell spreading on VCAM-1 are targ

79 nd CCL19 chemokines, as well as MAdCAM-1 and VCAM-1 cell-adhesion molecules.

80 attenuated TNF-alpha induction of ICAM-1 and VCAM-1 expression in GPx-1-deficient and control cells,

81 ion of sepsis-induced endothelial ICAM-1 and VCAM-1 expression in this model.

82 hosphorylation and an increase in ICAM-1 and VCAM-1 expression.

83 C4 upregulated the expressions of ICAM-1 and VCAM-1 in an aspirin-sensitive and TP receptor-dependent

84 and macrophage chemoattractant protein-1 and VCAM-1 levels in insulin-resistant LMCs indicated activa

85 signals, showing upregulation of ICAM-1 and VCAM-1 on their surface, as well as release of CCL2, sol

86 ulation of the adhesion molecules ICAM-1 and VCAM-1 resulted in an increased adhesion of peripheral b

87 their putative counter receptors ICAM-1 and VCAM-1 significantly attenuated CCL3-, CXCL1-, or PAF-el

88 xpression of the integrin ligands ICAM-1 and VCAM-1, as well as the T cell chemokines CXCL9, CXCL10,

89 F-alpha-activated endothelium and ICAM-1 and VCAM-1.

90 cells, as well as to immobilized ICAM-1 and VCAM-1.

91 NF-kappaB-dependent expression of ICAM-1 and VCAM-1.

92 ed, namely the adhesion molecules ICAM-1 and VCAM-1; the chemokines CCL5, CCL20, CXCL1, CXCL3, CXCL5,

93 s, stromal cell-derived factor 1 (SDF-1) and VCAM-1, which could be selectively blocked using a speci

94 as CXCL-9, CCL-20, CCL-4, CCL-2, ICAM-1, and VCAM-1 in HUVECs.

95 the greater expression of CCL19, ICAM-1, and VCAM-1 in the mucosal tip compared with the neuroepithel

96 38(++) PCs through secreted CXCL10/IP-10 and VCAM-1 contact.

97 tion, and inflammatory markers TNF-alpha and VCAM-1 expression.

98 the secretion of VCAM-1; both TNF-alpha and VCAM-1 were significantly associated with lower placenta

99 gnate endothelial receptors (alphaVbeta3 and VCAM-1).

100 In this study, we show that CCRL2 and VCAM-1 are upregulated on cultured human and mouse vascu

101 NTES), CCR7, CXCR4, GM-CSF, CD40, CD40L, and VCAM-1.

102 G myocardium had more inflammatory cells and VCAM-1-positive vessels than did wild-type myocardium af

103 appropriately in response to fibronectin and VCAM-1 binding.

104 beta(1)-mediated adhesion to fibronectin and VCAM-1 of lymphoma cell lines and primary CLL cells.

105 nic factors, which enhanced inflammation and VCAM-1 expression.

106 ion of angiopoietin 1, the c-Kit ligand, and VCAM-1.

107 ent MSCs did not induce T cell migration and VCAM-1 expression, resulting in insufficient cell-cell c

108 Osteopontin and VCAM-1 demonstrated sustained upregulation at all time p

109 s indicated that the source of periostin and VCAM-1 was the inflamed sheep liver tissue.

110 ic T cells required a chemokine response and VCAM-1 expression by the islets.

111 We also show that E-selectin and VCAM-1, but not ICAM-1, are upregulated in response to B

112 through an increase in TLR4, E-selectin, and VCAM-1 and ultimately through enhanced leukocyte recruit

113 ited the BMP9-induced expression of TLR4 and VCAM-1 and inhibited BMP9-induced human neutrophil recru

114 Increased ERK1/2 activity antagonizes VCAM-1 expression by repressing TNF induction of the tra

115 We have previously demonstrated that an anti-VCAM-1 antibody conjugated to microparticles of iron oxi

116 perfusion and, hence, ischemia, because anti-VCAM-1 significantly reduced the increased expression of

117 Intraocular injection of anti-VCAM-1 antibody eliminated the excessive ischemia-induce

118 crease in binding affinity and restored anti-VCAM-1 binding in tissue sections from ApoE(-)/(-) mice

119 ce expression of adhesion molecules (such as VCAM-1 the ligand for VLA-4), and leukocyte adhesion to

120 ly significant associations between baseline VCAM-1 or tumor necrosis factor alpha receptor 1 levels

121 ic or pharmacological FAK inhibition blocked VCAM-1 expression during development.

122 ral HIF-1-responsive genes caused in part by VCAM-1-induced worsening of nonperfusion and, hence, isc

123 d inhibited by 70% lipopolysaccharide-caused VCAM-1 expression in mice.

124 ral and dermal MVECs, and CXCL8, CCL3, CCL4, VCAM-1, and cyclooxygenase 2 (COX-2) in cerebral MVECs.

125 Rolling of hMSCs is regulated by CD29/VCAM-1, whereas CD29/CD44 interactions with VCAM-1, fibr

126 asting cellular contacts by enhancing T cell VCAM-1 expression in a CCL2-dependent manner.

127 Early up-regulation of cerebrovascular VCAM-1 expression was evident on tumor-associated vessel

128 Chronic VCAM-1 expression reflected the effect of platinum-based

129 AGEs N(epsilon)-(carboxymethyl)lysine (CML), VCAM-1, neutrophilic granulocytes, lymphocytes, and macr

130 surgical indication in the presence of CML, VCAM-1 expression, inflammatory cells, and fibrosis.

131 In a third set (n = 21), we compared VCAM-1 expression with (99m)Tc-cAbVCAM1-5 uptake in vari

132 In contrast, VCAM-1 was essential only for promoting endothelial-leuk

133 re distinct functional sites that coordinate VCAM-1 activation of calcium fluxes and Rac1 during leuk

134 murine cremasteric arterioles and decreased VCAM-1 and ICAM-1 expression.

135 on by blood endothelial cells, and decreased VCAM-1 while increasing CXCL1, CXCL2, CXCL12, CCL5, CCL2

136 ECFCs transfusion dramatically decreased VCAM-1 and NF-kappaB expression, increased eNOS expressi

137 Insulin decreased VCAM-1 expression and leukocyte adhesion in quiescent tu

138 lone, whereas antiatherogenic TGRL decreased VCAM-1 expression by approximately 20% while still upreg

139 We detected VCAM-1 on cholangiocytes in chronic liver disease (CLD)

140 ct of antiatherogenic TGRL by downregulating VCAM-1 expression.

141 When we silenced either VCAM-1 or M-CSFR in mice with myocardial infarction or i

142 platinum-resistant tumors retained elevated VCAM-1 expression and tumor burden after treatment.

143 ed with an impaired induction of endothelial VCAM-1 and led to a significantly reduced number of matu

144 y required for VEGF-A-stimulated endothelial VCAM-1 gene expression.

145 These results establish VCAM-1 and VAP-1 as mediators of myeloid cell recruitmen

146 within-pair analyses, all biomarkers, except VCAM-1, were higher in twins with lower CFR than their b

147 titis C), and human cholangiocytes expressed VCAM-1 in response to tumor necrosis factor alpha alone

148 women with advanced stage disease expressed VCAM-1, the incidence of expression was reduced among wo

149 monocytes to inflamed endothelium expressing VCAM-1 contributes to the development of plaque during a

150 a 2-fold increase in P-selectin expression, VCAM-1 expression, and platelet adhesion between 30 and

151 ng antibodies against von Willebrand factor, VCAM-1, and alpha-smooth muscle actin, were measured for

152 29, but not S730 or S737, were necessary for VCAM-1 activation of calcium fluxes.

153 37, but not S728 or Y729, were necessary for VCAM-1 activation of Rac1.

154 uce cytokines and/or chemokines required for VCAM-1 upregulation on the lung endothelium, which in tu

155 reduced expression of NF-kappaB target genes VCAM-1, intercellular adhesion molecule-1, E-selectin, a

156 tigen-positive vasculature displayed greater VCAM-1 intensity in patients with short duration of untr

157 bition concentration [IC50 ] 4 nM) and HUVEC VCAM-1 up-regulation (IC50 12 nM) in a dose-dependent ma

158 vant VCAM-1-specific imaging probes identify VCAM-1 expression as an indicator of ovarian cancer peri

159 ian cancer peritoneal metastasis to identify VCAM-1 as a viable imaging target.

160 boplatin resulted in a transient decrease in VCAM-1 expression 4 h after treatment that returned to b

161 il As was associated with a 1.7% increase in VCAM-1 (95% CI: 0.2, 3.2).

162 receptors and partly prevented increases in VCAM-1 and leukocyte adhesion after treatment with tumou

163 chemokines and adhesion molecules, including VCAM-1, IL-6, ICAM-1, E-selectin, and monocyte chemoattr

164 Toll-like receptor (TLR) 4 pathway increased VCAM-1 and ICAM-1 dependent binding of leukocytes.

165 ammatory Paigen diet significantly increased VCAM-1 expression with respect to the control group in v

166 nt BMSCs greatly compromised their increased VCAM-1 protein expression and IL-6 and RANKL secretion i

167 y, this change was correlated with increased VCAM-1 and phospho-IkBalpha immunoreactivity along the e

168 down-regulation is associated with increased VCAM-1 in both muscle and blood, suggesting that VCAM-1

169 XR agonists also prevented TNF-alpha-induced VCAM-1 and ICAM-1 expression, as well as endothelial gro

170 -GTP selectively decreased TNF-alpha-induced VCAM-1 but not ICAM-1 protein levels.

171 l FAK inhibition prevented TNF-alpha-induced VCAM-1 expression within heart vessel-associated endothe

172 iption factor required for TNF-alpha-induced VCAM-1 production.

173 n, these molecules suppressed ox-LDL-induced VCAM-1 expression and monocyte adhesion onto human endot

174 BI3 subunit with IL-35, promoted LPS-induced VCAM-1 in human aortic ECs and that EBI3-deficient mice

175 ticles from LPS-stimulated platelets induced VCAM-1 production by cultured human endothelial cells, a

176 ability of rapamycin to inhibit TNF-induced VCAM-1 expression.

177 educed endothelial expression of TNF-induced VCAM-1, which was restored via pharmacological inhibitio

178 n inhibitor of epoxide hydrolysis, inhibited VCAM-1 and ICAM-1 expression and protein levels; convers

179 id cells through an alpha(4)beta(1) integrin/VCAM-1-dependent mechanism.

180 We investigated VCAM-1 expression as a marker of peritoneal metastasis a

181 ulting in shear-resistant adhesion to ligand VCAM-1.

182 ve expression of the alpha(4)beta(1) ligand, VCAM-1, on the bronchioles, allowing direct access of th

183 mary progenitor cells to alpha4beta1 ligands VCAM-1 and CS1 under both static and flow conditions.

184 y roles for kinase-inhibited FAK in limiting VCAM-1 production via nuclear localization and promotion

185 activation by suppressing MAPK-AP1-mediated VCAM-1 expression and attenuates LPS-induced secretion o

186 The effects of carboplatin on mesothelial VCAM-1 expression were determined in cultured cells by W

187 n of endothelial cell (EC) adhesion molecule VCAM-1 through IL-35 receptors gp130 and IL-12Rbeta2 via

188 these macrophages use the adhesion molecule VCAM-1 to retain HSCs in the spleen.

189 ariation in vascular cell adhesion molecule (VCAM-1) expression correlates with the wall shear stress

190 E-selectin, vascular cell adhesion molecule (VCAM-1), and intercellular adhesion molecule 1 (ICAM-1)

191 -responsive genes such as adhesion molecules VCAM-1 and E-selectin in ECs in vitro and in vivo.

192 ma vascular and cellular adhesion molecules (VCAM-1 and ICAM-1, respectively), matrix metalloproteina

193 ptoglobin and CRP), cell adhesion molecules (VCAM-1), endothelial growth factors (VEGF) and VDBP.

194 zer p47phox, thereby increasing ROS-NFkappaB-VCAM-1/ICAM-1 expression and monocyte adhesion in ECs in

195 a consequence of artery ligation, whereas no VCAM-1 expression was detected in the contralateral caro

196 The data also suggest that antagonism of VCAM-1 provides a potential therapy to combat worsening

197 c cells induced the high-affinity binding of VCAM-1/CD106 Fc chimeric protein and promoted VCAM-1-dep

198 etinal NV that were abrogated by blockade of VCAM-1 included increases in leukostasis, influx of bone

199 Depletion of VCAM-1 interrupted the binding of macrophages to GBM cel

200 ide (VCAM-MPIO) enables in vivo detection of VCAM-1 by MRI.

201 n reported whether the cytoplasmic domain of VCAM-1 is necessary for these signals.

202 riptional and posttranscriptional editing of VCAM-1.

203 ly attenuated TNFalpha-induced expression of VCAM-1 and ICAM-1, and thus reduced monocyte adherence t

204 ndings indicate that in HCAECs expression of VCAM-1 and monocyte adhesion depend, to a significant ex

205 and hypothesized that biliary expression of VCAM-1 contributes to the persistence of liver inflammat

206 Expression of VCAM-1 in the ligated and contralateral carotid arteries

207 examined whether cholangiocyte expression of VCAM-1 promotes the survival of intrahepatic alpha4beta1

208 Importantly, expression of VCAM-1 was shown in human brain tissue containing both e

209 s enhanced gene and/or protein expression of VCAM-1, IL-6, and receptor activator of NF-kappaB ligand

210 Proatherogenic TGRL increased expression of VCAM-1, intercellular adhesion molecule 1 (ICAM-1), and

211 itive area and intensity/high power field of VCAM-1 expression than did juvenile DM patients with lon

212 In vivo imaging of VCAM-1 also demonstrated an acute decrease in expression

213 vatives might allow the molecular imaging of VCAM-1 expression in an experimental model of atheroscle

214 io was suboptimal for the in vivo imaging of VCAM-1 expression in atherosclerotic lesions.

215 otracer for the in vivo molecular imaging of VCAM-1 expression in atherosclerotic plaques.

216 Induction of VCAM-1 is dependent on tumor cell-clot formation, decrea

217 Simultaneous inhibition of VCAM-1 and VAP-1 does not result in further reduction in

218 patobiliary inflammation where inhibition of VCAM-1 decreased liver inflammation by reducing lymphocy

219 lerotic lesions correlated with the level of VCAM-1 expression (P < 0.05).

220 First, the relationship between the level of VCAM-1 expression and (99m)Tc-cAbVCAM1-5 uptake was eval

221 EDE levels of VCAM-1, von Willebrand factor, platelet-derived growth f

222 ensitive, and reproducible quantification of VCAM-1 expression in mouse atherosclerotic lesions.

223 sions of HO-1 and VEGF, and the reduction of VCAM-1.

224 d both ALK1 and ALK2 in the up-regulation of VCAM-1 and ICAM-1.

225 TGRL exerted this differential regulation of VCAM-1 by reciprocally modulating expression and activit

226 mental role for EGF-induced up-regulation of VCAM-1 expression in EGFR activation-promoted macrophage

227 We investigated the acute regulation of VCAM-1 expression in human aortic endothelial cells (HAE

228 y ER stress genes abrogated SS regulation of VCAM-1 transcription and monocyte recruitment.

229 atherogenic or antiatherogenic regulation of VCAM-1.

230 The miRNA miR-126, a negative regulator of VCAM-1 expression, was significantly decreased (3.39-fol

231 We examined the role of VCAM-1/alpha4beta1 integrin interaction in T cell recrui

232 alpha, which then triggered the secretion of VCAM-1; both TNF-alpha and VCAM-1 were significantly ass

233 lyzed VEGF-A isoform-specific stimulation of VCAM-1 gene expression, which controls endothelial-leuko

234 observations support testing the utility of VCAM-1 imaging probes to monitor treatment response in o

235 ooperation in shear-resistant cell arrest on VCAM-1 are ill defined.

236 itated the rolling and spreading of cells on VCAM-1 and the migration of cells toward SDF-1alpha.

237 of lymphatic endothelial cells; dependent on VCAM-1 and non-canonical NFkappaB signalling via LTbetaR

238 for leukocyte transendothelial migration on VCAM-1.

239 ta1-VCAM-1 interaction and cell spreading on VCAM-1 are targets of regulation by these three proteins

240 ignificant inhibition of T cell spreading on VCAM-1.

241 s, whereas ERK1/2 inhibition attenuated only VCAM-1 expression.

242 ein expression of PECAM-1, but not ICAM-1 or VCAM-1.

243 ological blockade of integrin alpha4beta1 or VCAM-1 inhibits it.

244 diated firm adhesion involving ICAM-1 and/or VCAM-1 and demonstrated ICAM-1-dependent shape-change an

245 in 2 genetic models lacking either Spi-C or VCAM-1 with impaired native macrophage proliferative exp

246 alized with antibodies to MAdCAM-1 (MB-M) or VCAM-1 (MB-V), biomarkers of gut endothelial cell inflam

247 ation with concomitant loss in E-selectin or VCAM-1 induction.

248 n, gauged by higher levels of IkBalpha, p65, VCAM-1, ICAM-1, CXCL10, CCL2, TNF, and IL-6 (mostly loca

249 tion into the CNS parenchyma and parenchymal VCAM-1 expression, and increased abluminal levels of CXC

250 In AF patients, VCAM-1 expression in blood vessels and the numbers of in

251 ocked by Abs against human LFA-1 and porcine VCAM-1.

252 c cells, necrotic cores, and proinflammatory VCAM-1 (vascular cell adhesion molecule) and MCP-1 (mono

253 CAM-1/CD106 Fc chimeric protein and promoted VCAM-1-dependent arrest to immobilized ligands under she

254 Radiolabeled VCAM-1-specific peptide imaging probes and SPECT were us

255 the integrin alpha4 and its counter-receptor VCAM-1, respectively; expression of the latter was upreg

256 ith platinum-sensitive tumors showed reduced VCAM-1 expression, which correlated with reduced tumor b

257 aked at 2 dynes/cm(2), where IRF-1-regulated VCAM-1 expression and monocyte recruitment also rose to

258 othelial CREB and significantly up-regulated VCAM-1, ICAM-1, and CXCL8.

259 esting a role for chemotherapy in regulating VCAM-1 expression.

260 Clinically relevant VCAM-1-specific imaging probes identify VCAM-1 expressio

261 Robust VCAM-1 immunostaining was observed in the left carotid a

262 lpha (P=0.0085); Fas-R (P=0.0354), and serum VCAM-1 (P=0.0007) were highly significant.

263 macrophages in CD169 iDTR mice or silencing VCAM-1 in macrophages released HSCs from the spleen.

264 lasminogen activator inhibitor-1 and soluble VCAM-1 associated with arsenic exposure were stronger am

265 igratory responsiveness to SDF-1 and soluble VCAM-1, which are among the chemokines and proteins foun

266 se of CCL2, soluble fractalkine, and soluble VCAM-1.

267 as alpha4beta1 integrin affinity for soluble VCAM-1 was not.

268 The HR for a 1-SD higher soluble VCAM-1 level was 1.34 (95% CI, 1.11-1.62; Bonferroni-cor

269 riable odds ratios for a 1-SD higher soluble VCAM-1 level, 1.91; 95% CI, 1.24-2.96, P = .003; and 2.5

270 Levels of soluble VCAM-1, but not other inflammation markers, are signific

271 ely associated with plasma levels of soluble VCAM-1.

272 rsenic (ln mug/g creatinine), plasma soluble VCAM-1 was 1.02 (95% confidence interval: 1.01, 1.03) an

273 uture studies should address whether soluble VCAM-1 is capable of improving AF risk classification be

274 -stimulation by CXCL12 together with soluble VCAM-1 potentiated integrin immobilization with a 5-fold

275 lenic macrophage maturation, reduced splenic VCAM-1 expression and compromised splenic HSC retention.

276 ATF-2 knockdown blocked VEGF-A-stimulated VCAM-1 expression and endothelial-leukocyte interactions

277 ric of EC orientation, markers of ER stress, VCAM-1 and ICAM-1 expression, and monocyte recruitment.

278 t increase in the expression of cell surface VCAM-1 (Akt-dependent) and ICAM-1 in Akt-dependent and e

279 on and tumor cell invasion and indicate that VCAM-1 is a potential molecular target for improving can

280 These results indicate that VCAM-1/alpha4beta1 integrin interaction is crucial for p

281 -1 in both muscle and blood, suggesting that VCAM-1 plays a critical role early in juvenile DM diseas

282 he VCAM-1 cytoplasmic domain, we deleted the VCAM-1 cytoplasmic domain or mutated the cytoplasmic dom

283 computational model of the structure of the VCAM-1 cytoplasmic domain as an alpha-helix with S728 an

284 restingly, the 19-amino acid sequence of the VCAM-1 cytoplasmic domain is 100% conserved among many m

285 To examine the function of the VCAM-1 cytoplasmic domain, we deleted the VCAM-1 cytopla

286 These VCAM-1 signals are required for leukocyte transendotheli

287 hyaluronan but had no effect on adhesion to VCAM-1 (alpha4beta1 integrin ligand), confirming its spe

288 to enhancement of VLA-4-mediated adhesion to VCAM-1.

289 by alpha4beta1 integrin-mediated adhesion to VCAM-1.

290 is, (99m)Tc-cAbVCAM1-5 specifically bound to VCAM-1-positive lesions, thereby allowing their identifi

291 , Swap-70(-/-) eosinophils adhered poorly to VCAM-1 and ICAM-1 and exhibited inefficient leading edge

292 n on foamy monocytes competent to recruit to VCAM-1 on inflamed arterial endothelium.

293 those in LPS-treated animals with respect to VCAM-1 or CD41 expression and lacked proliferation abnor

294 derived peptide B2702p bound specifically to VCAM-1 and allowed the ex vivo imaging of atheroscleroti

295 vation of endothelial cells (EC) upregulates VCAM-1 receptors that target monocyte recruitment to ath

296 Metastases were detectable in vivo using VCAM-1-targeted MRI 5 d after induction (<1,000 cells).

297 from cytokinestimulated HBEC to T cells was VCAM-1 and ICAM-1 dependent.

298 ur objectives here were to determine whether VCAM-1 is up-regulated on vessels associated with brain

299 ed with brain metastases, and if so, whether VCAM-1-targeted MRI enables early detection of these tum

300 /VCAM-1, whereas CD29/CD44 interactions with VCAM-1, fibronectin, and hyaluronan on HSECs determine f