ライフサイエンスコーパス: HUVEC

1 HUVEC (but not HMEC-1) upregulate expression of TGF-beta

2 HUVEC ATPase activity increased by 25% with cilostazol a

3 HUVEC oxygen consumption and superoxide and hydrogen per

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

5 HUVEC were incubated with human whole blood.

6 HUVEC were reliant on glycolysis and FAO, and inhibition

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 exposed to EF (162 mV/mm at 1.2 Hz) and moni

12 HUVECs were treated with and without palmitate in the pr

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

14 etabolism and the gamma-glutamyl cycle in 62 HUVEC strains carrying different rs10911021 genotypes.

15 -60 cells (i) binding to TNF-alpha-activated HUVEC with a concurrent reduction in endothelial cell ad

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

17 We further apply Qdots to analyze HUVEC heterogeneity and observe that 24 h VEGF-A(165) tr

18 id not exert cytotoxic effects on Caco-2 and HUVEC cells (viability was >80%).

19 dependently decreased the growth of A549 and HUVEC cells.

20 Human bone marrow stromal cell (HBMSC) and HUVEC spheroids were implanted within a bone defect site

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

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

23 This study found that in mice and HUVEC models, exposure to ATO led to CAPN-1 activation b

24 esis in chorioallantoic membranes (CAMs) and HUVECs.

25 2 and P-selectin, in breast cancer cells and HUVECs, and antibodies against these integrins efficient

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

27 nd endothelial cells (ECs) (iPSC-derived and HUVECs).

28 y passaged human brain microvascular ECs and HUVECs with high MW Abeta1-42 oligomers (5 uM, for 72 h)

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

30 ithin the cell spheres containing HBMSCs and HUVECs, and CD31-positive cell clusters were prominent w

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

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

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

34 endogenous CD146 that is highly expressed by HUVEC.

35 nd C5a increase C3aR and C5aR1 expression by HUVECs as well as directing their cellular transmigratio

36 rment in proliferation and tube formation by HUVECs.

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

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

39 ) and Human Umbilical Vein Endothelial Cell (HUVEC) 3D fibrin gel model.

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

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

42 of a human umbilical vein endothelial cell (HUVEC)-lined, perfusable, bioengineered blood vessel and

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

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

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

46 CRBN knock down in human endothelial cells (HUVEC and HMVEC-L), did not affect endothelial cell prol

47 sing human umbilical vein endothelial cells (HUVEC) and differentiated neutrophil-like HL-60 (dHL-60)

48 mary human umbilical vein endothelial cells (HUVEC) and immortalized human microvascular endothelial

49 genesis, and apoptosis of endothelial cells (HUVEC) and on osteoblast mineralization of vascular smoo

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

51 mary human umbilical vein endothelial cells (HUVEC) and used time-lapse videomicrosopy and quantitati

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

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

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

55 d on human umbilical vein endothelial cells (HUVEC) in vitro.

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

57 A in human umbilical vein endothelial cells (HUVEC) that may mediate these effects.

58 rove Human Umbilical Vein Endothelial Cells (HUVEC) tube regression and apoptosis in vitro.

59 and human umbilical vein endothelial cells (HUVEC) with SHIP-1 knockdown were analyzed in TGF-beta1

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

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

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

63 like human umbilical vein endothelial cells (HUVEC).

64 and Human Umbilical Vein Endothelial Cells (HUVEC).

65 with human umbilical vein endothelial cells (HUVEC).

66 lasts (WI-38, IMR-90) and endothelial cells (HUVEC, HAEC) by replicative exhaustion, exposure to ioni

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

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

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

70 mary human umbilical vein endothelial cells (HUVECs) and aortic endothelial cells (HAoECs) we show th

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

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

73 human umbilical vascular endothelial cells (HUVECs) and examined how C3a or C5a activation of HUVECs

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

75 ured human umbilical vein endothelial cells (HUVECs) and SC cells were transduced with adenovirus con

76 , in human umbilical vein endothelial cells (HUVECs) and skin fibroblasts.

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

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

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

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

81 s of human umbilical vein endothelial cells (HUVECs) for the specific endonucleolytic cleavage of a t

82 Human umbilical vein endothelial cells (HUVECs) formed dense networks on the sheets when co-cult

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

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

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

86 with human umbilical vein endothelial cells (HUVECs) in gelatin methacrylate (GelMA) hydrogel.

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

88 n in human umbilical vein endothelial cells (HUVECs) in vitro, followed by quantitative RT-PCR analys

89 t on human umbilical vein endothelial cells (HUVECs) increased cell viability and decreased oxidative

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

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

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

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

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

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

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

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

98 and human umbilical vein endothelial cells (HUVECs) treated with ATO.

99 Human umbilical vein endothelial cells (HUVECs) treated with dextrin confirmed eNOS uncoupling,

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

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

102 4 in human umbilical vein endothelial cells (HUVECs) using shRNA also inhibited flow-induced alignmen

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

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

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

106 ) or human umbilical vein endothelial cells (HUVECs) with recombinant VEGF triggered a robust increas

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

108 mary human umbilical vein endothelial cells (HUVECs), HUVEC-derived EA.hy926 cells, and human dermal

109 ured human umbilical vein endothelial cells (HUVECs), PAI-1 and eNOS colocalize and proximity ligatio

110 In human umbilical vein endothelial cells (HUVECs), the risk allele "C" is associated with lower ex

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

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

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

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

115 with human umbilical vein endothelial cells (HUVECs).

116 with human umbilical vein endothelial cells (HUVECs).

117 human umbilical vascular endothelial cells (HUVECs).

118 and human umbilical vein endothelial cells (HUVECs).

119 2 on human umbilical vein endothelial cells (HUVECs).

120 mary human umbilical vein endothelial cells (HUVECs).

121 ting human umbilical vein endothelial cells (HUVECs).

122 eted human umbilical vein endothelial cells (HUVECs).

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

124 umor spheroids containing MDA-MB-231 cells + HUVECs in an HLF-laden, fibrin-based ECM within our micr

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

126 In coherent HUVECs, RCalphabeta reinforced the actin cytoskeleton an

127 macromolecular transport through a confluent HUVEC monolayer.

128 ration through TNF-alpha-activated confluent HUVEC monolayer by stabilizing VE-cadherin and beta-cate

129 ease in R(Cell) of EF stimulated and control HUVECs after 54 h and 78 h, respectively.

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

131 paired ATAC-seq and RNA-seq data on cultured HUVECs under hypoxic and normoxic conditions.

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

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

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

135 at GMVECs had greater AP activation than did HUVECs.

136 genesis patterns of Human Umbilical Vein EC (HUVEC).

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

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

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

140 rmal or HG treated human umbilical vein ECs (HUVECs).

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

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

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

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

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

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

147 various tri-culture protocols of NRVCM:hASC:HUVEC and found that a ratio of 1,500,000:37,500:150,000

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

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

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

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

152 m cells (MSCs)/human lung fibroblasts (HLFs)/HUVECs) and the extracellular matrix (ECM: collagen, Mat

153 n umbilical vein endothelial cells (HUVECs), HUVEC-derived EA.hy926 cells, and human dermal microvasc

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

155 -223 expression in plasma EV, thus improving HUVEC angiogenesis and reducing VSMC calcification.

156 In HUVEC monolayers, flux analysis revealed that VEGF-A pro

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

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

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

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

161 SHIP-1 knockdown in HUVEC cells resulted in enhanced EndoMT induced by BLM.

162 that lead candidates inhibit tube length in HUVEC cells.

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

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

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

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

167 ds of genes were differentially regulated in HUVEC as compared to HMEC-1.

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

169 ion required both TAB1-TAB2 and TAB1-TAB3 in HUVEC.

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

171 data, causally linked the loss of ERK1/2 in HUVECs in vitro to activation of TGFbeta signaling, EndM

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

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

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

175 criptional mechanism involving miR-219-5p in HUVECs.

176 aits associated with the 1q25 risk allele in HUVECs, including impairments of the gamma-glutamyl cycl

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

178 otensive and hypertensive rat vessels and in HUVECs.

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

180 scular endothelial cadherin (VE-cadherin) in HUVECs in response to ATO were partially mitigated by tr

181 Knock-down of CARD8 in HUVECs significantly altered proteins involved in inflam

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

183 and mRNA stability of DDAH1 but not DDAH2 in HUVECs, whereas overexpression of NRP1 increased the mRN

184 revent oxLDL-induced cellular dysfunction in HUVECs.

185 We investigated whether UA induced EndoMT in HUVECs and an animal model of hyperuricemia fed with 2%

186 UA induced EndoMT in HUVECs with a generation of reactive oxygen species via

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

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

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

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

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

192 n of interleukin 8 triggered by histamine in HUVECs.

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

194 rough in-vitro live cell imaging of NF-kB in HUVECs exposed to different flow conditions, stochastic

195 confirmed the colocalization observations in HUVECs.

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

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

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

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

200 , they did not change glycocalyx shedding in HUVECs.

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

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

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

204 ce the formation of transcellular tunnels in HUVECs.

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

206 patients reduced angiogenesis and increased HUVEC apoptosis and VSMC calcification; however, all the

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

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

209 oved the role of this microRNA in EV-induced HUVEC and VSMC dysfunction.

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

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

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

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

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

215 utomer confirmed this activity and inhibited HUVEC proliferation with an IC(50) of 1.9 muM.

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

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

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

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

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

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

222 bsence of Tks4 also decreases the ability of HUVEC cells to form multicellular sprouts, a key require

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

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

225 he structural integrity and functionality of HUVEC-lined microfluidic channels.

226 Nevertheless, incubation of HUVEC cells with melanoidins from common bread and biscu

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

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

229 tudy characterised the metabolic response of HUVEC to the PPARbeta/delta agonist, GW0742, and compare

230 rradiated PolyRad inhibited the viability of HUVEC in a dose-dependent manner.

231 s) and examined how C3a or C5a activation of HUVECs affects the activation and polarization of lympha

232 irect regulatory role in the angiogenesis of HUVECs.

233 sing 4 genome-wide mRNA expression arrays of HUVECs during normoxia and after 2, 8, and 16 h of hypox

234 Importantly, exposure of HUVECs to sheer stress inhibited YK-4-279-induced apopto

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

236 inhibited the proliferation and migration of HUVECs in vitro.

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

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

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

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

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

242 to beta2-GPI was detected on the surface of HUVECs, and colocalization of MBL with beta2-GPI was obs

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

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

245 Treatment of HUVECs with longistatin prior to stimulation substantial

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

247 SLURP1 suppresses neutrophil (i) docking on HUVEC cells by decreasing endothelial cell adhesion mole

248 1beta had similar, albeit lesser, effects on HUVEC gene expression, and it only slightly affected GMV

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

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

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

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

253 urement of 1 100 VEGFR1 and 6 900 VEGFR2 per HUVEC.

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

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

256 on depended on TAB1-TAB2, whereas in primary HUVECs, both TAB1-TAB2 and TAB1-TAB3 were required for p

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

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

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

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

261 Only VEGF-A stimulated HUVEC migration and proliferation whereas both GW0742 an

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

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

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

265 impaired NO production in insulin-stimulated HUVECs.

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

267 In response to high shear stress, HUVECs and SC cells expressed more SEAP and GFP than con

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

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

270 esis were further confirmed in HHSEC and the HUVEC 3D fibrin gel model, respectively.

271 ease was seen in BV in femurs containing the HUVEC and HBMSC monocell constructs.

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

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

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

275 ctin production, (ii) transmigration through HUVEC monolayer by stabilizing endothelial cell membrane

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

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

278 adhesion molecules and monocyte adherence to HUVECs.

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

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

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

282 at facilitated cancer cell chemotaxis toward HUVECs.

283 nflammatory cytokines (25-50%) in HG treated HUVECs and HG-CM.

284 Satellite cells grown in CM from HG treated HUVECs reduced growth (25%), differentiation (25%) and m

285 ase in HMuSC treated with CM from HG treated HUVECs.

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

287 potent inducer of glycolysis in tubulogenic HUVEC, while FAO was maintained.

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

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

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

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

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

293 neutrophil chemotaxis, and interaction with HUVEC.

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

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

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

299 mulated breast cancer cell interactions with HUVECs.

300 positive cell clusters were prominent within HUVEC-implanted defects.