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 peaked at 2 dynes/cm(2) and decreased to below st

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

8 VCAM-1 was expressed and secreted by murine and human pa

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 dependent vascular cell adhesion molecule 1 (VCAM-1) expression on lung endothelial cells.

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

14 tegrin to vascular cell adhesion molecule 1 (VCAM-1) on neurons in the inflammatory context.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

31 ession of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1),

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

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

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

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

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

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

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

39 First, vascular adhesion molecule-1 (VCAM-1) was evaluated as a vascular target of inflammati

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

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

42 AM-1) and vascular cell adhesion molecule-1 (VCAM-1), are expressed.

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

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

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

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

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

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

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

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

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

52 y and vascular inflammation (p65, caspase 1, VCAM [vascular cell adhesion molecule-1], ICAM [intercel

53 kines, such as CD31, BDNF, TFF3, Serpin E-1, VCAM-1, Vitamin D BP, and PDGF-AA, were significantly up

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

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

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

57 emic and vascular inflammation (CRP, ICAM-1, VCAM-1), and SAA (all P < .001).

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

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

60 g and activation proteins, including ICAM-1, VCAM-1, HLA class I and II, and interferon gamma recepto

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

62 1-targeted nanocarriers outperformed PECAM-1/VCAM-1 in control and disease-like conditions, and tripl

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

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

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

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

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

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

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

70 ta extract, or rIL-33 was used to induce AAI/VCAM-1 expression in wild-type (WT) and RAGE-knockout (R

71 ain-enhancer of activated B cells) activity, VCAM, ICAM, and MCP1 levels in hypertensive subjects com

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

73 1 and Hemopexin among Caucasians, and ALCAM, VCAM-1, TFPI and PF-4 among Asians.

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

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

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

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

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

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

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

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

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

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

84 ctional expression of endothelial ICAM-1 and VCAM-1 was confirmed by T-cell interaction with EECM-BME

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

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

87 ry molecules such as IL-6, MCP-1, ICAM-1 and VCAM-1.

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

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

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

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

92 Mechanistically, MMP-9 and VCAM-1 appear to be involved downstream of PDGF-PDGFRbet

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

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

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

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

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

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

99 ed levels of the adhesion molecules ICAM and VCAM and the pattern-recognition receptors TLR7 and TLR9

100 led to significant augmentation of ICAM and VCAM expression, elevated leukocyte adhesion to and migr

101 ion and decreased CNS T cell infiltrates and VCAM-1+ endothelial cells.

102 roglia, Th1 and Th17 T cell infiltrates, and VCAM-1+ endothelial cells and improved neurocognitive ac

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

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

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

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

107 tive disease are ALCAM, PF-4, properdin, and VCAM-1 among African-Americans, sE-selectin, VCAM-1, BFL

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

109 ed cell surface expression of P-selectin and VCAM-1.

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

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

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

113 Anti-VCAM-1 coated rods exhibited a 3.5-fold increase in the

114 Anti-VCAM/LNP selectively accumulated in the inflamed brain,

115 Anti-VCAM/LNP-mRNA mediated expression of thrombomodulin (a n

116 y to vascular cell adhesion molecule 1 (anti-VCAM) in the inflamed brain is >10-fold greater than ant

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

118 metry showed that in the inflamed brain anti-VCAM/liposomes bind to endothelium, not to leukocytes.

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

120 Furthermore, uptake of anti-VCAM/liposomes exceeded that of anti-TfR and anti-ICAM c

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

122 ed tomography imaging affirmed specific anti-VCAM/liposome targeting to inflamed brain in mice.

123 Intravenous (i.v.) anti-VCAM-1 or intraperitoneal (i.p.) beta7 blocking antibody

124 dhesion, nanoparticles were coated with anti-VCAM-1 and tested under static conditions in cell cultur

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

126 pression or knock-down of VCAM-1, as well as VCAM-1-blocking treatment in the spontaneous mouse model

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

144 Endothelial VCAM-1 surface expression stimulated by TNFalpha provide

145 s beta1-integrin (VLA-4) to bind endothelial VCAM-1.

146 cts produced TGRL that increased endothelial VCAM-1 expression by >=35%, and exhibited impaired fasti

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

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

149 Enhanced VCAM-1 expression in the lungs by HDM, AA, or rIL-33 exp

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

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

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

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

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

155 Finally, FAK/Pyk2 activity is required for VCAM-1 expression and macrophage recruitment to the vess

156 IP-10, GM-CSF, M-CSF, TNF-alpha, IFN-gamma, VCAM-1, ICAM-1, PD-L1 and ICOS-L.

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

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

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

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

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

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

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

164 evented this response as well as increase in VCAM-1, ICAM-1, IL-6, and IL-8 levels.

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

166 adhesion molecule (CAM) expression including VCAM-1, ICAM-1, and E-selectin in human aortic endotheli

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

168 caused decreased NOS activity and increased VCAM-1 expression in RAECs.

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

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

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

172 se lung endothelial cells with IL-33 induced VCAM-1 expression in WT, but not RAGE-KO cells.

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

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

175 nstrates that allergen- and cytokine-induced VCAM-1 expression is RAGE-dependent and contributes to l

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

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

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

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

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

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

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

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

184 or IFN regulatory factor 1, promoted maximum VCAM-1 expression.

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 ssion of the endothelial activation molecule VCAM-1 but increased expression of the endothelial tight

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

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

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

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

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

193 PS)-induced vascular cell adhesion molecule (VCAM) protein levels by ~50%, whereas the monomeric D73K

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

195 TbetaR) and vascular cell adhesion molecule (VCAM), but not intercellular adhesion molecule (ICAM), s

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

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

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

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

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

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

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

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

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

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

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

207 Administration of VCAM-1 and beta7-integrin blocking antibodies reduced IL

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

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

210 tumors with overexpression or knock-down of VCAM-1, as well as VCAM-1-blocking treatment in the spon

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

212 Differential expression of VCAM-1 and intercellular adhesion molecule 1 (ICAM-1) wa

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

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

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

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

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

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

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

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

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

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

223 ed medium further increased the induction of VCAM-1.

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

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

226 Moreover, the pharmacological inhibition of VCAM-1 in Phc2-deficient mice reverses the symptoms.

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

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

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

230 these metabolites was strongly predictive of VCAM-1 expression.

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

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

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

234 Endothelial up-regulation of VCAM-1 at susceptible sites in arteries modulates the re

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

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

237 atherogenic or antiatherogenic regulation of VCAM-1.

238 nistration was used to determine the role of VCAM-1 in IL-33-induced AAI.

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

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

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

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

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

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

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

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

247 by 1-NM-PP1 enhanced eosinophil spreading on VCAM-1 but inhibited eotaxin-1 (CCL11)-mediated eosinoph

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

249 (PF-228 or Dasatinib), which inhibited only VCAM-1 expression.

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

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

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

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

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

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

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

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

258 p38 specifically abrogated the rise to peak VCAM-1 at low SS (2 dyn/cm(2)), whereas inhibition of ER

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

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

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

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

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

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

265 %, whereas the monomeric D73K mutant reduced VCAM by 90% at the same concentration.

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

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

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

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

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

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

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

273 VCAM-1 among African-Americans, sE-selectin, VCAM-1, BFL-1 and Hemopexin among Caucasians, and ALCAM,

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

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

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

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

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

279 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

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

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

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

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

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

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

286 riptional regulation of TNF-alpha-stimulated VCAM-1 expression.

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

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

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

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

291 Thus VCAM-directed nanocarriers provide a platform for cerebr

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

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

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

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

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

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

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

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

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