ライフサイエンスコーパス: HUVEC

1 HUVEC ATPase activity increased by 25% with cilostazol a

2 HUVEC intercellular adhesion molecule-1 expression, stif

3 HUVEC migration (P = 0.01) and vessel tube formation (P

4 HUVEC oxygen consumption and superoxide and hydrogen per

5 HUVEC responded to TNF-alpha and Stx2a by increasing pro

6 HUVEC were incubated with human whole blood.

7 HUVEC, endothelial cells derived from blood progenitors

8 HUVEC-conditioned medium was sufficient to enhance axona

9 HUVEC: PMN co-cultures were perfused for additional 15 m

10 HUVECs expressed elevated CD39 protein (2-fold [P<0.05]

11 HUVECs were treated with and without palmitate in the pr

12 mbrane advance agreed with experiments of 3D HUVEC migration at r(2) > 0.95 for diverse ECMs with dif

13 own to exert antiangiogenic activity against HUVEC cells and anticancer efficacy against several canc

14 dependently decreased the growth of A549 and HUVEC cells.

15 h-attenuated transcytosis through HEK293 and HUVEC monolayers, and less leptospires in blood, lung, l

16 proinflammatory molecules in both HRCEC and HUVEC.

17 to when exposed to noncancerous (MCF10A and HUVEC) cells.

18 % inhibition concentration [IC50 ] 4 nM) and HUVEC VCAM-1 up-regulation (IC50 12 nM) in a dose-depend

19 esis in chorioallantoic membranes (CAMs) and HUVECs.

20 2 and P-selectin, in breast cancer cells and HUVECs, and antibodies against these integrins efficient

21 thelial carcinoma cells, Ishikawa cells, and HUVECs with IL-17A revealed significant increase in angi

22 -bound thrombin was decreased, in GMVECs and HUVECs exposed to TNF.

23 active enhancers, in unstimulated HUVECs and HUVECs stimulated with VEGFA for 1, 4, and 12 h.

24 aving typical membrane compositions, such as HUVEC and erythrocytes, is low.

25 of human cells, SSV2 differentiates between HUVECs and hCMEC/D3 cells, thus opening a path for selec

26 In an in vitro human system, CD47 on both HUVEC and T cells was required for TEM.

27 inase and the expression of beta-Pix in both HUVECs and tumor cell lines.

28 UVECs from infants who survived without BPD, HUVECs obtained from infants who developed BPD or died h

29 endogenous CD146 that is highly expressed by HUVEC.

30 Vascular structures formed by HUVECs in vitro were successfully anastomosed with the h

31 ofound in HUVEC mono-cultures; whilst in C3A:HUVEC co-culture, cells were less susceptible to the tox

32 HC.HA also caused HUVECs to become small and rounded, with a decrease in s

33 bited human umbilical vein endothelial cell (HUVEC) migration and tube formation by suppressing VEGFR

34 and a human umbilical vein endothelial cell (HUVEC) model.

35 with human umbilical vein endothelial cell (HUVEC) monolayers, which were activated with tumor necro

36 moted human umbilical vein endothelial cell (HUVEC) proliferation through inhibiting DLL4-directed No

37 , and human umbilical vein endothelial cell (HUVEC) vascular cell adhesion molecule 1 (VCAM-1) upregu

38 mplexes show inhibition of endothelial cell (HUVECs) proliferation, indicating their antiangiogenic n

39 on in human umbilical vein endothelial cell (HUVECs), challenged with high D-glucose (60% inhibition)

40 ty in human umbilical vein endothelial cell (HUVECs), which was reflected in increased angiogenesis i

41 s in human umbilical vein endothelial cells (HUVEC) and Schlemm's canal (SC) endothelial cells with A

42 eproduced in normal human endothelial cells (HUVEC) at concentrations double those effective in tumor

43 and human umbilical vein endothelial cells (HUVEC) by stimulating expression of proinflammatory mole

44 and human umbilical vein endothelial cells (HUVEC) cultured in triple-negative MDA-MB-231 tumor-cond

45 ying human umbilical vein endothelial cells (HUVEC) differentiation assay and chicken chorioallantoic

46 s in human umbilical vein endothelial cells (HUVEC) following FXa-mediated PAR activation and investi

47 Human umbilical vein endothelial cells (HUVEC) grown on laminar-flow perfusion channels were sti

48 n of human umbilical vein endothelial cells (HUVEC) in vitro.

49 and human umbilical vein endothelial cells (HUVEC) were transduced with recombinant adenoviral vecto

50 n cultured human vascular endothelial cells (HUVEC), and a cell proliferation kit (WST-8) was used to

51 ly), human umbilical vein endothelial cells (HUVEC), as well as primary human hepatocytes and hepatic

52 d by human umbilical vein endothelial cells (HUVEC), leading to the accumulation of platelet-derived

53 vitro in human umbilical endothelial cells (HUVEC), resulting in the phosphorylation of endothelial

54 and Human Umbilical Vein Endothelial Cells (HUVEC).

55 with human umbilical vein endothelial cells (HUVEC).

56 human umbilical vascular endothelial cells (HUVEC).

57 HRGEC) and umbilical vein endothelial cells (HUVEC).

58 like human umbilical vein endothelial cells (HUVEC).

59 n of human umbilical vein endothelial cells (HUVECs) (p<0.01) and the angiogenesis induced by basic f

60 of PGE2 in human vascular endothelial cells (HUVECs) although the amount of extracellular PGE2 was no

61 e between human umbilical endothelial cells (HUVECs) and a human melanoma cell line (Lu1205) increase

62 Firstly, human umbilical endothelial cells (HUVECs) and Colon 26 NL-17 mouse carcinoma cells were tr

63 with human umbilical vein endothelial cells (HUVECs) and enhancing tube stability up to 6 days in vit

64 with human umbilical vein endothelial cells (HUVECs) and human coronary artery endothelial cells (HCA

65 n of human umbilical vein endothelial cells (HUVECs) and neovascularization in chicken chorioallantoi

66 atterns showed that human endothelial cells (HUVECs) are repulsed by HTPCs.

67 sing human umbilical vein endothelial cells (HUVECs) as a model system.

68 sing human umbilical vein endothelial cells (HUVECs) as model of tumor endothelial cells.

69 and human umbilical vein endothelial cells (HUVECs) as previously reported.

70 ured human umbilical vein endothelial cells (HUVECs) by real-time PCR: C3 and C5; complement factor (

71 l as human umbilical vein endothelial cells (HUVECs) developed a SASP that could be suppressed by tar

72 and human umbilical vein endothelial cells (HUVECs) encapsulated in 5% gelatin methacrylate (GelMA)

73 Human umbilical vein endothelial cells (HUVECs) formed focal adhesion complexes on RGD- and RGD

74 ects human umbilical vein endothelial cells (HUVECs) from oxidised LDL (oxLDL)-mediated dysfunction i

75 Human umbilical vein endothelial cells (HUVECs) grown in microfluidic devices were treated with

76 ized human umbilical vein endothelial cells (HUVECs) grown on Transwell membranes.

77 d by human umbilical vein endothelial cells (HUVECs) in pulp regeneration.

78 xtract via human vascular endothelial cells (HUVECs) indicates that the corrosion products are well t

79 n of human umbilical vein endothelial cells (HUVECs) induces a transcriptional induction of the proan

80 y in human umbilical vein endothelial cells (HUVECs) is sensitive to blockers of Ca(2+) release-activ

81 Human umbilical vein endothelial cells (HUVECs) may contribute to the study of vascular repair a

82 In human umbilical vein endothelial cells (HUVECs) Ned-19 abolished VEGF-induced Ca(2+) release, im

83 n in human umbilical vein endothelial cells (HUVECs) obtained from extremely preterm infants were ass

84 cted human umbilical vein endothelial cells (HUVECs) resembling EndoMT were monitored by qPCR, immuno

85 ere, we report that human endothelial cells (HUVECs) secrete brain-derived neurotrophic factor (BDNF)

86 ting human umbilical vein endothelial cells (HUVECs) to low oxygen, mimicking a characteristic of neo

87 mary human umbilical vein endothelial cells (HUVECs) to study their ability to induce activation of T

88 d in human umbilical vein endothelial cells (HUVECs) upon transfection with miR-K6-5 and during KSHV

89 and human umbilical vein endothelial cells (HUVECs) using genome-wide global run-on sequencing (GRO-

90 4 in human umbilical vein endothelial cells (HUVECs) using shRNA also inhibited flow-induced alignmen

91 l of human umbilical vein endothelial cells (HUVECs) was investigated.

92 Human umbilical vein endothelial cells (HUVECs) were cultured with or without Mn(2+) supplementa

93 Human endothelial cells (HUVECs) were incubated with (18)F-FDG or (18)F-FLT and c

94 and human umbilical vein endothelial cells (HUVECs) were treated with the PDE3 inhibitors cilostazol

95 ated human umbilical vein endothelial cells (HUVECs) with E2, TNFalpha, or both and found that E2 cou

96 from human umbilical vein endothelial cells (HUVECs), and Stx2B can cause thrombotic microangiopathy

97 r on human umbilical vein endothelial cells (HUVECs), and that ZIKV uses AXL with much greater effici

98 Human umbilical vein endothelial cells (HUVECs), aortic smooth muscle cells, HeLa cells, HEK293

99 mary human umbilical vein endothelial cells (HUVECs), HEK 293 cells and cancer cells.

100 lture with human vascular endothelial cells (HUVECs), thus demonstrating biocompatibility and relevan

101 sing human umbilical vein endothelial cells (HUVECs), we explored mechanisms underlying the requireme

102 with human umbilical vein endothelial cells (HUVECs).

103 human umbilical vascular endothelial cells (HUVECs).

104 and human umbilical vein endothelial cells (HUVECs).

105 y of human umbilical vein endothelial cells (HUVECs).

106 appreciably toxic toward endothelial cells (HUVECs).

107 pression by human venular endothelial cells (HUVECs).

108 n of human umbilical vein endothelial cells (HUVECs).

109 e to human umbilical vein endothelial cells (HUVECs).

110 with human umbilical vein endothelial cells (HUVECs).

111 F-7 and MDA-MB-435) over noncancerous cells (HUVECs and MCF-10A).

112 In vitro, human umbilical vein cells (HUVECs) subjected to GR knockdown by siRNA showed increa

113 ll line, HepG2, and human endothelial cells, HUVECs, as well as ex vivo and in vivo models have been

114 macromolecular transport through a confluent HUVEC monolayer.

115 the FSHR expression in human umbilical cord, HUVECs or immortalized HUVECs (HUV-ST).

116 d the RAGE V domain, and stimulated cultured HUVECs adhered to a longistatin-coated surface; this bin

117 The results showed that SFN decreased HUVEC cell viability, migration and tube formation, all

118 -selectin-dependent function: CD63-deficient HUVECs fail to recruit leukocytes, CD63-deficient mice e

119 Live-cell imaging of Erg-deficient HUVECs showed a reduction in lamellipodia, in line with

120 Consistent with these results, S4-depleted HUVECs in long-term laminar flow showed increased activa

121 at GMVECs had greater AP activation than did HUVECs.

122 s) from these mice, and human umbilical ECs (HUVEC) treated with Kindlin-2 siRNA showed enhanced basa

123 e-transcriptome in human umbilical vein ECs (HUVECs) and found that ALK1 signaling inhibition was ass

124 cells) and primary human umbilical vein ECs (HUVECs) under 4 dyn/cm(2) laminar shear stress for 24 h

125 e bodies (WPBs) in human umbilical vein ECs (HUVECs), human aortic ECs (HAECs), and human heart micro

126 ressed on cultured human umbilical vein ECs (HUVECs), increasing NP uptake through clathrin-coated pi

127 Here, using human umbilical vein ECs (HUVECs), we report that extracellular Ca(2+) is required

128 In endothelial HUVECs, gemcitabine, bevacizumab, sunitinib and EMAP cau

129 n in vitro human umbilical vein endothelial (HUVEC) and BV2 cell co-culture model.

130 In all cells tested--except HUVECs where expression was not modulated by interferon-

131 TIE2-L914F-expressing HUVECs formed VMs with ectatic blood-filled channels tha

132 In cultured TIE2-L914F-expressing HUVECs, rapamycin effectively reduced mutant TIE2-induce

133 Conversely, direct FCSC-HUVEC contact significantly enhanced the osteogenic diff

134 proliferation, whereas OSR1 is required for HUVEC chemotaxis and invasion.

135 ET-1 was induced to a greater extent from HUVECs than from breast cancer cells, resulting in a den

136 ls and showed that LEC support tumor growth, HUVEC have no significant effect on tumor growth, wherea

137 ssues formed in G1, GelMA encapsulated hDPSC/HUVEC-filled RSs, and less cellularized host cell-derive

138 Of importance, only the G1, hDPSC/HUVEC-encapsulated GelMA constructs formed pulp cells th

139 l analysis showed that GelMA supported hDPSC/HUVEC cell attachment and proliferation and also provide

140 identify GelMA hydrogel combined with hDPSC/HUVECs as a promising new clinically relevant pulpal rev

141 human umbilical cord, HUVECs or immortalized HUVECs (HUV-ST).

142 spherical tips, E (kPa) was 0.71 +/- 0.16 in HUVEC and 0.94 +/- 0.06 in SC cells.

143 measured using sharp tips: 3.23 +/- 0.54 in HUVEC and 6.67 +/- 1.07 in SC cells.

144 ascular disrupting activity was evaluated in HUVEC cells, with compound 3c showing activity comparabl

145 Similar experiments in HUVEC showed that UK14304 prevented the activation-depen

146 reduction in axonal growth when incubated in HUVEC-conditioned medium and in direct co-culture with H

147 nhanced phosphorylation of PI3/Akt kinase in HUVEC, endothelial cell wound healing, and tube formatio

148 ll invasion, and decreases neovasculature in HUVEC and also tumor volume in EAT mouse models.

149 es with prominent cortices (312 +/- 65 nm in HUVEC and 371 +/- 91 nm in SC cells).

150 inophen (APAP) toxicity was most profound in HUVEC mono-cultures; whilst in C3A:HUVEC co-culture, cel

151 tion, wound healing or cell proliferation in HUVEC/HUV-ST.

152 FXa-mediated intracellular Ca(2+) release in HUVEC and FXa reactive IgG from patients with APS and/or

153 In HUVECs ionizing radiation induces TGIF1 expression as we

154 In HUVECs lacking GR, NF-kappaB levels and NF-kappaB-depend

155 In HUVECs, tacrolimus activated Smad1/5/8 and opposed the p

156 In HUVECs, TNF-alpha- and radiation-induced NF-kappaB pathw

157 CCL-20, CCL-4, CCL-2, ICAM-1, and VCAM-1 in HUVECs.

158 howed high specificity for alpha V beta 3 in HUVECs (K d 35 nM).

159 is indicated that inhibition of miRNA-429 in HUVECs up-regulated 209 mRNAs, a number of which regulat

160 explore the potential function of miR-497 in HUVECs by using MTT and TUNEL assays.

161 rovascular endothelial cells (GMVECs) and in HUVECs, a frequently used investigational model of endot

162 receptor to activate Akt for angiogenesis in HUVECs and that CXCR7 may be a potential target molecule

163 nist, SNC80, did not prevent angiogenesis in HUVECs.

164 ed that gene expression of CCNE2 and CDC6 in HUVECs was downregulated after SsnB exposure, to 64% and

165 iled to promote ICAM-1 expression changes in HUVECs on contact.

166 revent oxLDL-induced cellular dysfunction in HUVECs.

167 ed that VGSCalpha proteins were expressed in HUVECs, and immunohistochemistry revealed VGSCalpha expr

168 Inhibition of Erg expression in HUVECs resulted in decreased migration in vitro, while E

169 his cell type, we induced GILZ expression in HUVECs via transient transfection.

170 e significant induction of tube formation in HUVECs and in vivo.

171 tion, migration and colony tube formation in HUVECs associated with the phosphorylation of ERK and AK

172 smigration and eliminating hole formation in HUVECs on stiff substrates.

173 Endothelial tube formation in HUVECs was increased when co-cultured with PGE2-conditio

174 WNK1 is required for cord formation in HUVECs, but the actions of the two major WNK1 effectors,

175 the expression and functionality of FSHR in HUVECs angiogenesis, and were unable to reproduce the FS

176 nsive chromatin interaction map generated in HUVECs using tethered conformation capture (TCC) and cha

177 n of interleukin 8 triggered by histamine in HUVECs.

178 d activation of ERK1/2, JNK, p38 and IKKs in HUVECs.

179 Knockdown of NCX1 (the main NCX isoform in HUVECs) by siRNA confirmed the pharmacological data.

180 nal VGSC alpha- and beta-subunit isoforms in HUVECs were Nav1.5, Nav1.7, VGSCbeta1, and VGSCbeta3.

181 and caspase-3 activation induced by oxLDL in HUVECs.

182 x2B activate different signaling pathways in HUVECs.

183 and corresponding CD141 surface presence in HUVECs and GMVECs were reduced, and gene expression of c

184 Large-scale miRNA profiling in HUVECs identified miR-92a as an atheromiR candidate, who

185 s resulted in induction of ICAM-1 protein in HUVECs.

186 Epidermal growth factor (EGF) receptor in HUVECs was LeY modified.

187 MCP-1 secretion, and ICAM-1 up-regulation in HUVECs treated with HG.

188 ing the anti-inflammatory Slit2 and Robo4 in HUVECs in vitro, as well as in arterial endothelial cell

189 e angiogenic functions and VEGF signaling in HUVECs.

190 otes an endothelial dysfunction signature in HUVECs that is characterized by transcription suppressio

191 We report that FIH-1 silencing in HUVECs results in reduced growth and increased apoptosis

192 Our studies in HUVECs show that ox-LDL induced autophagy and damaged mt

193 ey inhibitor of apoptosis), FIH targeting in HUVECs leads to selective repression of survivin in endo

194 ce the formation of transcellular tunnels in HUVECs.

195 erse but complementary approaches, including HUVEC-mediated trophoblast invasion in nude mice, in vit

196 IL-25 increased HUVEC proliferation and the number, length, and area of

197 a significantly decreased capacity to induce HUVEC proliferation and aortic sprouting.

198 We observed a Galectin-1-induced HUVEC apoptosis in a dose-dependent manner as demonstrat

199 expression, compared with MatLu and induced HUVEC, respectively, based on flow cytometry detecting a

200 (-4) muCi/mL) for LNCaP, Mat-Lu, and induced HUVEC, respectively, which are comparable to the values

201 rs of HUVEC induced to express PSMA (induced HUVEC).

202 on occurs through modulation of VEGF-induced HUVEC depolarization and [Ca(2+)](i).

203 Finally, NCX inhibitors reduced VEGF-induced HUVEC proliferation, migration, and tubular differentiat

204 verexpression of miR-497 effectively induced HUVECs apoptosis by targeting VEGFR2 and downstream PI3K

205 y experiment, FCSC cell feeder layer induced HUVECs to form significantly shorter and less sprouts th

206 produced in insect cells, they also infected HUVECs in an AXL-dependent manner.

207 response study identified the drugs inhibit HUVEC cell proliferation in vitro, and also target the d

208 re, we generated a model of VMs by injecting HUVECs expressing the most frequent VM-causing TIE2 muta

209 mensional capillary tube formation involving HUVEC and/or HTR8 trophoblasts, and aortic ring endothel

210 We found that EndoMT occurs in irradiated HUVECs with concomitant Hey2 mRNA and protein increase.

211 lar results were observed in MnSOD knockdown HUVECs following Mn(2+) supplementation, suggesting that

212 DG/(18)F-FLT or (18)F-FDG/(18)F-FLT-labelled HUVECs, following the surgical induction of mouse hind-l

213 line (SKOV3ip1) and endothelial cell lines (HUVEC & SVEC4-10).

214 PI3K --> Akt --> FAK, by which TR3 mediates HUVEC migration.

215 of >150 images to quantify the attachment of HUVEC-released complement proteins to ULVWF strings secr

216 Rescue of A-1254-induced disruption of HUVEC-based tube formation by gamma-secretase inhibitor

217 Using (18)F-FLT-labelling, estimation of HUVEC retention within the engraftment site 4 hr post-ad

218 P and rat Mat-Lu cells) and on monolayers of HUVEC induced to express PSMA (induced HUVEC).

219 cells increased the angiogenic potential of HUVEC in a paracrine fashion; conversely, knockdown of R

220 to aqueous mAbs/fragments in the presence of HUVEC monolayers.

221 sed in a redox-active form at the surface of HUVEC and acts as an inhibitor of complement deposition

222 lation of ERK upon LPS plus S1P treatment of HUVEC and human aortic endothelial cells and cell-type d

223 esis in vivo, and decreased the viability of HUVEC (Human Umbilical Vein Endothelial Cells) cells in

224 Flow cytometric cell cycle analysis of HUVECs treated with SsnB showed an increase of cells in

225 irect regulatory role in the angiogenesis of HUVECs.

226 sent study, we demonstrated that exposure of HUVECs to HIV Tat protein resulted in induced expression

227 ibiting cell migration and tube formation of HUVECs in vitro.

228 Incubation of HUVECs with StxB transiently increased phospholipase D (

229 inhibited the proliferation and migration of HUVECs in vitro.

230 S-Fc specifically inhibited the migration of HUVECs, human dermal lymphatic ECs, and the HT29, HCT116

231 tion was observed during the polarization of HUVECs in stripe assays.

232 le-like flow conditions, the pretreatment of HUVECs, but not neutrophils, with alpha2-agonists decrea

233 lated the following angiogenic properties of HUVECs: VEGF-induced proliferation or chemotaxis, tubula

234 The cellular responses of HUVECs on TiO2 nanofibrous surfaces were studied through

235 ube networks and growth factors secretion of HUVECs, as well as leading to higher expression level of

236 Stimulation of HUVECs with sublytic complement concentrations evoked WP

237 Transfection of HUVECs with miR-132 enhances growth factor-induced proli

238 Transfection of HUVECs with miR-132 NP resulted in a 2-fold increase in

239 Treatment of HUVECs with longistatin prior to stimulation substantial

240 urthermore, IL-17A promoted tubulogenesis of HUVECs plated on Matrigel in a dose-dependent manner.

241 ) was used to measure the effect of IL-25 on HUVEC proliferation.

242 1beta had similar, albeit lesser, effects on HUVEC gene expression, and it only slightly affected GMV

243 rcellular adhesion molecule-1) expression on HUVEC (human umbilical vein endothelial cells) in vitro.

244 ount for the dependence of transmigration on HUVEC substrate stiffness.

245 ine stimulation enhanced LICOS expression on HUVECs and ICOS-LICOS interaction up-regulated ICOS expr

246 cule 1 (ICAM-1) and E-selectin expression on HUVECs by 3- and 1.5-fold, respectively, compared with H

247 responsible for the ICAM-1 up-regulation on HUVECs.

248 were separately co-cultured with MSCs and/or HUVECs.

249 , basal, and regulated pathways in polarized HUVECs, and have established a new role for AP-1 in the

250 urther enhanced using cytokine prestimulated HUVECs.

251 ia, we followed HIF1A mRNA levels in primary HUVECs over 24 hours using quantitative PCR.

252 ol 12-myristate 13-acetate (PMA), in primary HUVECs was found to require PKCeta- and PKCepsilon-depen

253 In this study, we show that, in primary HUVECs, Slit2 represses LPS-induced secretion of certain

254 e current study, ADAM10 knockdown on primary HUVECs was found to impair transmigration of freshly iso

255 FSH-FSHR signaling was shown to promote HUVEC angiogenesis and thereafter suggested to have an i

256 g expression of a reporter gene in recipient HUVEC.

257 Remarkably, HUVEC cells naturally migrated in the ECM scaffold and s

258 tly, SFN markedly supressed HepG2-stimulated HUVEC migration, adhesion and tube formation; which may

259 Additionally, NAC stimulated HUVEC migration and proliferation in a phospholipase C b

260 MPs were generated from TNF-alpha-stimulated HUVECs and quantified by using flow cytometry.

261 impaired NO production in insulin-stimulated HUVECs.

262 In thrombin-stimulated HUVECs, Kindlin-2 and cortical actin dissociated from st

263 antly reduced the capacity of TNF-stimulated HUVECs to support leukocyte rolling, adhesion, and trans

264 HC.HA suppressed HUVEC viability more significantly than HA and AM stroma

265 We found that HUVEC-released C4 did not attach to ULVWF strings, rulin

266 We found that HUVECs transfected with miR-K6-5 had increased Rac1-GTP

267 These data show that HUVECs secrete neurotrophic factors that significantly e

268 In the HUVEC model, FAE, quercetin-3-O-glucoside and quercetin-

269 irectional polarization and migration in the HUVECs, which is necessary for tube formation.

270 e monophosphate (cAMP) to vary the Pd of the HUVECs monolayer towards fluorescent polystyrene NPs (pN

271 at miR-499 had antiangiogenic effects on the HUVECs and suppressed the secretion of vascular endothel

272 WF strings secreted by, and anchored to, the HUVECs (under conditions of ADAMTS-13 inhibition).

273 th CORM-401 did not suppress PMN adhesion to HUVEC, but significantly reduced PMN transendothelial mi

274 When LPS Exos or I/L Exos were added to HUVECs, we found a significant increase in adhesion mole

275 adhesion molecules and monocyte adherence to HUVECs.

276 so stimulated breast cancer cell adhesion to HUVECs and transendothelial migration, which were repres

277 n caused a reduction in monocyte adhesion to HUVECs treated with HG or MCP-1.

278 c1-GTP levels and tube formation compared to HUVECs transfected with control miRNAs.

279 T cells need direct cell-to-cell contact to HUVECs to induce proliferation.

280 of polymorphonuclear and tumor cell lines to HUVECs; thus, we suggested that ICOS-Fc may act as an an

281 at facilitated cancer cell chemotaxis toward HUVECs.

282 ng endogenous GILZ in glucocorticoid-treated HUVECs did not alter their capacity to support leukocyte

283 , and tube formation was blocked by treating HUVECs with an Akt inhibitor.

284 marker of active enhancers, in unstimulated HUVECs and HUVECs stimulated with VEGFA for 1, 4, and 12

285 Using 70 kDa dextran as a probe, untreated HUVECs yielded a Pd that approximated tumor vasculature

286 ferences in secreted VEGF were assayed using HUVEC migration.

287 f brain (hCMEC/D3 cells) and umbilical vein (HUVEC) origin.

288 of pro-angiogenic structures in an in vitro HUVEC culture model.

289 ta1/pSMAD3 signaling, also decrease in vitro HUVEC endothelial tube formation and inhibit BMP9 bindin

290 In vitro, HUVEC constitutively expressed IL-25R, which was up-regu

291 When HUVECs are exposed to the bacterial toxin EDIN, which ca

292 A similar response was absent when HUVECs were cocultured with podocytes, indicating a tiss

293 Pd that approximated tumor vasculature while HUVECs treated with 25 mug/mL cAMP had Pd that approxima

294 Similar results were obtained with HUVEC and HTR8 trophoblasts.

295 Coincubation of the spirochete with HUVEC or HEK293 cells directly caused the significant el

296 ocultivation of TGN1412-treated T cells with HUVECs induced T-cell activation that was further enhanc

297 3- and 1.5-fold, respectively, compared with HUVECs alone.

298 Compared with HUVECs from infants who survived without BPD, HUVECs obt

299 itioned medium and in direct co-culture with HUVECs.

300 mulated breast cancer cell interactions with HUVECs.