ライフサイエンスコーパス: VCAM

1 VCAM levels increased by an average (standard deviation)

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

3 VCAM-1 and osteopontin demonstrated sustained upregulati

4 VCAM-1 expression by cholangiocytes contributes to persi

5 VCAM-1 expression correlated with tumor stage.

6 VCAM-1 expression detected by MRI increased significantl

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

59 (4.4-folds); decreased expression of ICAM-1, VCAM-1 (3.2-fold), along with reduced levels of cytokine

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

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

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

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

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

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

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

67 1-targeted nanocarriers outperformed PECAM-1/VCAM-1 in control and disease-like conditions, and tripl

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

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

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

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

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

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

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

75 In agreement, VCAM docking models suggest that binding of domain 1 of

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

77 asymmetric dimethyl-arginine (P < 0.001) and VCAM levels (P < 0.001) at 12 months were significantly

78 glomerular filtration rate (P = 0.027), and VCAM (P = 0.014) levels were the independent predictors

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

95 38(++) PCs through secreted CXCL10/IP-10 and VCAM-1 contact.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

112 resonance imaging (MRI) contrast agent [anti-VCAM-microparticles of iron oxide (MPIO)] to identify co

113 nti-IL-17A or IgG and two injections of anti-VCAM-MPIO before undergoing T2*-weighted three-dimension

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

145 29, but not S730 or S737, were necessary for VCAM-1 activation of calcium fluxes.

146 37, but not S728 or Y729, were necessary for VCAM-1 activation of Rac1.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

179 ICAM) 1 and vascular cell adhesion molecule (VCAM) 1 and for proper trafficking of lymphocytes to sec

180 the ligand vascular cell adhesion molecule (VCAM) for binding to cell surface alpha4beta1 shows nonc

181 tory marker vascular cell adhesion molecule (VCAM) in cells and animals challenged with the cytokine

182 erleukin-6, vascular cell adhesion molecule (VCAM), and asymmetric dimethylarginine levels were measu

183 pression of vascular cell adhesion molecule (VCAM)-1 in human cultured endothelial cells, under infla

184 , IL-8, and vascular cell adhesion molecule (VCAM)-1 were assessed by bead-based multiplex assay, and

185 e (ICAM)-1, vascular cell adhesion molecule (VCAM)-1, and activated leukocyte cell adhesion molecule

186 )-alpha; 4) vascular cell adhesion molecule (VCAM); 5) interleukin (IL)-6; 6) IL-8; 7) intercellular

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

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

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

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

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

192 ions of either quiescent or activated MuSCs (VCAM(+)CD31(-)CD45(-)Sca1(-)).

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

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

195 g models suggest that binding of domain 1 of VCAM to alpha4-integrins is unimpeded by the Fab, and th

196 ge in orientation between domains 1 and 2 of VCAM for binding to alpha4beta1.

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

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

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

200 riptional and posttranscriptional editing of VCAM-1.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

226 atherogenic or antiatherogenic regulation of VCAM-1.

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

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

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

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

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

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

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

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

235 for leukocyte transendothelial migration on VCAM-1.

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

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

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

239 nium-diethylenetriamine pentaacetic acid- or VCAM-MPIO-positive lesions during relapse.

240 icate that targeting integrin alpha4beta1 or VCAM to inhibit the interactions of tumor cells with the

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

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

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

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

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

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

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

248 Higher baseline urine VEGF and plasma VCAM levels correlated with worse PFS and overall surviv

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

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

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

252 ation and NF-kappaB translocation, promoting VCAM expression on endothelial cells and TNF-alpha relea

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

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

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

256 onal scores, and are associated with reduced VCAM-MPIO lesions during remission.

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

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

295 pathology is more sensitively detected using VCAM-MPIO MRI, which may, therefore, be used to monitor

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