ライフサイエンスコーパス: tube formation

1 ited lymphangiogenesis in an in vitro model (tube formation).

2 lmonary endothelial adhesion, migration, and tube formation.

3 antibody partially inhibited ET-1 effects on tube formation.

4 feration, cell migration, and capillary-like tube formation.

5 MECs), prior silencing of NEU1 did not alter tube formation.

6 uced LPS induced EC sprouting, migration and tube formation.

7 l nitric oxide synthase, cell migration, and tube formation.

8 ew new colonies could develop following germ tube formation.

9 counteracted NEU1-mediated inhibition of EC tube formation.

10 el role for Smad-like proteins in epithelial tube formation.

11 -2 induced EC marker expression and in vitro tube formation.

12 ding proliferation, migration, and capillary tube formation.

13 s upregulates PECAM1 expression and promotes tube formation.

14 regulates vasculogenesis through endothelial tube formation.

15 ed to increased migration, proliferation and tube formation.

16 GF-induced Ca(2+) release and capillary-like tube formation.

17 h abrogated the NEU1 inhibitory effect on EC tube formation.

18 ay and resulted in successful capillary-like tube formation.

19 -93 overexpression enhanced endothelial cell tube formation.

20 ne regulators of EC migration, invasion, and tube formation.

21 significant and dose-responsive increase in tube formation.

22 VEGF-induced endothelial cell migration and tube formation.

23 ributed to endothelial cell infiltration and tube formation.

24 kdown impairs endothelial cell migration and tube formation.

25 d that SPIN90/WISH is required for capillary tube formation.

26 vasion, adhesion, and VEGF-induced capillary tube formation.

27 f vascular permeability and endothelial cell tube formation.

28 d as the pathway responsible for p17-induced tube formation.

29 acizumab in the inhibition of HB-EGF-induced tube formation.

30 d adhesion to laminin, and impaired vascular tube formation.

31 and also induced endothelial cell capillary tube formation.

32 educed chemotherapy-induced endothelial cell tube formation.

33 enic effect of MEF2C knockdown on retinal EC tube formation.

34 LF as autocrine regulator of EC invasion and tube formation.

35 ls to restore endothelial cell sprouting and tube formation.

36 reduced HDMEC migration by 50% and abolished tube formation.

37 anisotropic partition of lipids, leading to tube formation.

38 induced HRMVEC DNA synthesis, migration, and tube formation.

39 te endothelial proliferation, migration, and tube formation.

40 ited 15(S)-HETE-induced HDMVEC migration and tube formation.

41 d after phosphorylation by PKA increases the tube formation.

42 gamma with RNAi attenuates the PGE2-induced tube formation.

43 thelial growth factor-induced capillary-like tube formation.

44 nd partially prevented CPX inhibition of LEC tube formation.

45 es of adhesion, proliferation, and capillary tube formation.

46 s required for the ability of PSG1 to induce tube formation.

47 ion in HDMVECs affecting their migration and tube formation.

48 gnaling, migration, adhesion, spreading, and tube formation.

49 R-3 mimicked the effect of CPX, blocking the tube formation.

50 oduction, cell proliferation, migration, and tube formation.

51 lyzed for the role of PLCgamma1 in promoting tube formation.

52 ration in the HUVECs, which is necessary for tube formation.

53 isms involved in folate action during neural tube formation.

54 odulation of HRMVEC migration, sprouting and tube formation.

55 impaired endothelial cell proliferation and tube formation.

56 of cell migration, invasion, and endothelial tube formation.

57 lial cells from apoptosis and restored their tube formation.

58 tic events including gastrulation and neural tube formation.

59 sed endothelial proliferation, migration and tube formation.

60 d human EPCs were analyzed for migration and tube formation.

61 othelial cells induced apoptosis and blocked tube formation.

62 reduced HRMEC migration, proliferation, and tube formation.

63 growing bundles as a dynamical bottleneck to tube formation.

64 uman endothelial cell (EC) proliferation and tube formation.

65 laments, significantly delaying bundling and tube formation.

66 elial cell (HRMVEC) migration, sprouting and tube formation.

67 mphatic endothelial cells (LECs) and inhibit tube formation.

68 amin E, by reducing 8-isoprostane, increased tube formation.

69 U inhibited cellular invasion, migration and tube formation.

70 67.1 +/- 33.4 vs. 205.0 +/- 13% at 48 h) and tube formation (7.7 +/- 1.1 vs. 1.6 +/- 0.5 tubes/field)

71 d VEGF(165) induced proliferation, capillary tube formation, activation of VEGFR2 and MMP2 in human u

72 These exosomes promoted tube formation activity in human umbilical vein endothel

73 VEGFA-induced DNA synthesis, migration, and tube formation, albeit more robustly with Kdr downregula

74 ecreased HUVEC cell viability, migration and tube formation, all of which are important steps in angi

75 omplete blockage prevent internalization and tube formation, although such manipulations affect the g

76 d also causes an even earlier block to heart tube formation and a bifid phenotype.

77 iferation, decreased apoptosis, but impaired tube formation and angiogenesis.

78 opic expression of miR-27a blocked capillary tube formation and angiogenesis.

79 r tyrosine kinases and Notch are crucial for tube formation and branching morphogenesis in many syste

80 effect of PRP was analysed by matrigel-based tube formation and by fibrous capsule formation assays.

81 ll proliferation and in vitro capillary-like tube formation and caused apoptosis of human umbilical v

82 at very low-range doses promoting migration, tube formation and cell invasion in bovine aortic endoth

83 Mimic 221 treatment resulted in reduced tube formation and cell migration, where as the reverse

84 ls synergized with K1 to facilitate vascular tube formation and cell proliferation, and enhance angio

85 ts synergized with vIL-6 to promote vascular tube formation and cell proliferation.

86 angiogenesis, we performed in vitro Matrigel tube formation and chemotaxis assays using human microva

87 and histone deacetylase 6 (HDAC6), blocks EC tube formation and cytoskeletal polarization, while siRN

88 It also inhibited cell tube formation and decreased in vitro invasion of tumor

89 can form outside the embryo, suggesting that tube formation and elongation are intrinsic properties o

90 C4 antibody perturbed tube formation and endothelial sprouting in vitro and in

91 or -3 inhibited endothelial cell vessel-like tube formation and extracellular matrix invasion, each o

92 esis, and relationships among farnesol, germ tube formation and hyphal maintenance.

93 ls induced rapidly in vitro endothelial cell tube formation and in vivo tumors after xenografting in

94 ng, also decrease in vitro HUVEC endothelial tube formation and inhibit BMP9 binding to recombinant E

95 siologic concentrations of ox-LDL stimulated tube formation and inhibited susceptibility to apoptosis

96 accharide (LPS)-activated macrophage-induced tube formation and its associated factors in endothelial

97 Folr1; also known as FRalpha) impairs neural tube formation and leads to NTDs.

98 reated HMVECs had decreased endothelial cell tube formation and migration compared with control siRNA

99 nduced retinopathy (OIR) model and inhibited tube formation and migration in cultured endothelial cel

100 d BMPER(-/-) endothelial cells have impaired tube formation and migratory ability compared with wild-

101 etion to levels sufficient to blunt in vitro tube formation and proliferation of endothelial cells.

102 for VEGFR-2-dependent endothelial capillary tube formation and proliferation.

103 that LeY is involved in vascular endothelial tube formation and rTMD1 inhibits angiogenesis via inter

104 292 inhibited cZNF292 expression and reduced tube formation and spheroid sprouting of endothelial cel

105 proliferation and migration, and to promote tube formation and sprouting of new vessels in a rat aor

106 rate that MEIS2 is critical for proper heart tube formation and subsequent cardiac looping.

107 hat JUN strongly stimulates endothelial cell tube formation and that DLL4 constrains this process.

108 Therefore, the role of LeY in tube formation and the role of the recombinant lectin-li

109 , endothelial cell proliferation, migration, tube formation and thereby, angiogenesis by suppressing

110 podia and facilitates endothelial migration, tube formation and vascular development in zebrafish tha

111 dothelial cell migration, sustained in vitro tube formation and vasorelaxation via the nitric oxide p

112 on of OATP2A1 function significantly reduced tube formation and wound-healing activity of PGE2 in hum

113 ellular survival, proliferation, endothelial tube formation and xenograft angiogenesis and growth.

114 ogenic properties (proliferation, migration, tube formation) and attenuated vascular endothelial grow

115 o endothelial cell proliferation, migration, tube formation, and activation of downstream angiogenic

116 iated EC proliferation, migration, capillary tube formation, and aortic ring-based angiogenesis.

117 endothelial cell invasion, proliferation and tube formation, and CatK deficiency is associated with d

118 ated by growth factor-induced proliferation, tube formation, and cell migration assays.

119 uction in adhesion, migration, survival, and tube formation, and decreased BMPR2 and downstream signa

120 esis was examined using in vitro chemotaxis, tube formation, and in vivo Matrigel plug assays.

121 ial cells, GHCer addition induces migration, tube formation, and intracellular Ca(2+) mobilization in

122 ll proliferation, migration, transmigration, tube formation, and production of pro-angiogenic factors

123 mediated receptor phosphorylation, capillary tube formation, and proliferation of endothelial cells c

124 o angiogenesis (including a tumor model), EC tube formation, and proliferation.

125 cell proliferation, survival, migration, and tube formation, and promotes lymphangiogenesis in vitro

126 anges assessed included adhesion, migration, tube formation, and propensity to apoptosis.

127 ll adhesion, migration, in vitro endothelial tube formation, and spheroid sprouting.

128 ion rescued high glucose-impaired migration, tube formation, and survival of BMCs or mature human car

129 ested EP4 mediates the prostaglandin-induced tube formation, and this conclusion was substantiated wi

130 oliferation, endothelial cell proliferation, tube formation, and VEGF production more effectively tha

131 ospondin-1, including blockade of migration, tube formation, and VEGFR-2 signaling in response to fib

132 ts neovascularization, indicated by in vitro tube-formation, aortic-ring, and coated-bead assays and

133 hereas NO donors or PDGFR antagonist reduced tube formation approximately 50% by murine and human MSC

134 that both IL-17-induced HMVEC chemotaxis and tube formation are mediated primarily through IL-17 rece

135 However, the timing and location of H-tube formation are unknown.

136 ls with miR-6126 mimic significantly reduced tube formation as well as invasion and migration capacit

137 ffects of 15(S)-HETE on HDMVEC migration and tube formation as well as Matrigel plug angiogenesis.

138 ed the effects of rapamycin on migration and tube formation as well as RhoA activation and cytoskelet

139 addition, C2238-alphaANP reduced endothelial tube formation, as assessed by matrigel.

140 resses in vitro migration, proliferation and tube formation, as well as in vivo angiogenesis and tumo

141 This tube formation assay is preferred, as other in vitro ass

142 cell death detection ELISA, transwell assay, tube formation assay, and CAM assay.

143 that of the control in the in vitro matrigel tube formation assay.

144 -angiogenic activity in the endothelial cell tube formation assay.

145 is in vitro was analysed using migration and tube formation assay.

146 urther evidenced by increased branching in a tube-formation assay and in vivo.

147 can inhibit cell motility and migration, and tube formation assays indicate that both can impede tubu

148 both in vitro and in vivo assays, including tube formation assays using human vascular endothelial c

149 Endothelial cell migration and tube formation assays were used to demonstrate the direc

150 analysis and endothelial cell chemotaxis and tube formation assays.

151 The results suggest that CPX inhibits LEC tube formation at least, in part, through inhibiting VEG

152 cell migration and disrupted capillary-like tube formation at noncytotoxic concentrations.

153 hi) PDA cells to (a) induce endothelial cell tube formation, (b) generate long ectopic blood vessels

154 EC) is sufficient to induce EC migration and tube formation but not proliferation, indicating that ST

155 in a paracrine manner to promote endothelial tube formation, but also act as autocrine growth factors

156 culture of LECs with TH2 cells also inhibits tube formation, but this effect is fully reversed by int

157 ), p150(Glued), and Clasp1, control human EC tube formation by (1) inducing microtubule assembly and

158 the NNE during the dynamic events of neural tube formation by both activating key epithelial genes a

159 nd suppressed VEGF-induced proliferation and tube formation by ECs.

160 of A-1254-induced disruption of HUVEC-based tube formation by gamma-secretase inhibitor L1790 confir

161 uced the induction of HMVEC migration and/or tube formation by RA synovial fluid.

162 vein endothelial cell (HUVEC) migration and tube formation by suppressing VEGFR2 expression.

163 ial cell viability, migration, adhesion, and tube formation by targeting IGF1R and Met signals.

164 h was required to promote cell migration and tube formation by VEGF-A.

165 exhibited augmented adhesion, migration, and tube formation capacities.

166 upting its integrity, and improving vascular tube formation capacity.

167 on in ECs significantly reduces or increases tube formation, cell migration, and cell differentiation

168 We show that endothelial cell migration, tube formation, cell sprouting from aortic rings, tumor

169 h miR-K6-5 had increased Rac1-GTP levels and tube formation compared to HUVECs transfected with contr

170 ulture system had decreased endothelial cell tube formation compared with control siRNA-treated HMVEC

171 molecular link underlying vertebrate neural tube formation, connecting planar cell polarity patterni

172 s in PGE(2) expression, HDMEC migration, and tube formation could be corrected by treatment with the

173 d the inhibitory effect of calcitriol on LEC tube formation, demonstrating how such inhibition is VDR

174 n allows the stabilization of capillary-like tube formation during latent infection, as the addition

175 n HUVEC, endothelial cell wound healing, and tube formation elicited by RCE and WCE suggest that over

176 They enhanced endothelial cell tube formation, endothelial cell sprouting from spheroid

177 EGF-A(165)-induced proliferation, migration, tube formation, formation of F-actin stress fiber, and i

178 smooth muscle cells (SMCs) and promoted the tube formation from ECs.

179 induced HRMVEC DNA synthesis, migration, and tube formation from inhibition by down-regulation of cPL

180 Angiogenesis was determined by in vitro tube formation from serum from each patient with or with

181 VEC-dNeo proliferation, migration, capillary tube formation, gene expression, and production of angio

182 d contributes myocardium after initial heart tube formation, giving rise to both smooth muscle and my

183 adhesion, cell proliferation, capillary-like tube formation, growth factors secretion (VEGF and BFGF)

184 a robustly induces endothelial migration and tube formation, hallmarks of angiogenesis.

185 y reduced CCL21-induced HMVEC chemotaxis and tube formation; however, suppression of the ERK and JNK

186 ring Drosophila gastrulation: (I) mesodermal tube formation, (II) collapse of the mesoderm, (III) dor

187 educed serum-induced HRMEC proliferation and tube formation in a dose-dependent manner.

188 d with E2 and G-1 promoted human endothelial tube formation in a GPER-dependent manner.

189 in endothelial cells diminished VEGF-induced tube formation in a three-dimensional collagen gel.

190 o limits VEGF expression, proliferation, and tube formation in ALK1-expressing endothelial cells.

191 of H(2)O(2,) whereas PEG-catalase attenuated tube formation in control LECs.

192 KSHV induces stabilization of capillary-like tube formation in cultured endothelial cells.

193 ctivated platelets caused cell migration and tube formation in cultured human endothelial cells and s

194 Tube formation in cultured Nox4(-/-) lung endothelial ce

195 and how this cellular process contributes to tube formation in different developmental contexts.

196 1), an increase in KS-associated phenotypes (tube formation in endothelial cells and vascular endothe

197 s compared to solvent controls, and decrease tube formation in endothelial cells.

198 tial (tube network on 2-dimensional culture, tube formation in growth factor reduced Matrigel) than n

199 The antagonist also blocked the rescue of tube formation in GSNOR(-/-) MSCs by L-NAME or the GHRH

200 s augmented VEGF-A production and normalized tube formation in GSNOR(-/-) MSCs, whereas NO donors or

201 st) resulted in the significant induction of tube formation in HUVECs and in vivo.

202 ncreased proliferation, migration and colony tube formation in HUVECs associated with the phosphoryla

203 Endothelial tube formation in HUVECs was increased when co-cultured

204 NT did not stimulate tube formation in isolated human intestinal macrovascula

205 rtial resistance to CPX inhibitory effect on tube formation in lymphatic endothelial cells (LECs), wh

206 longer-term stabilization of capillary-like tube formation in Matrigel, a basement membrane matrix.

207 gration, sprouting angiogenesis, and network tube formation in matrigel, whereas blockade of miR-26a

208 dothelial cell proliferation, migration, and tube formation in response to both VEGF- and basic fibro

209 ial proliferation, migration, and angiogenic tube formation in response to FGF-2.

210 ce displayed elevated cell proliferation and tube formation in response to VEGF stimulation.

211 cells count, endothelial cell migration, and tube formation in vascular endothelial growth factor A (

212 ng gastrulation in many organisms and neural tube formation in vertebrates.

213 (165)-induced endothelial cell sprouting and tube formation in vitro and FGF2-dependent angiogenesis

214 EGFA-induced HRMVEC migration, sprouting and tube formation in vitro and hypoxia-induced retinal endo

215 ation was found to increase with endothelial tube formation in vitro and in vivo during retinal neova

216 dothelial cell proliferation, migration, and tube formation in vitro and in vivo.

217 e synthetic ligand troglitazone also reduced tube formation in vitro and in vivo.

218 prostate fibroblasts stimulated endothelial tube formation in vitro and promoted tumor growth in mic

219 primary ECs arrested capillary sprouting and tube formation in vitro because of impaired adhesion and

220 ts suppressed endothelial cell migration and tube formation in vitro in response to VEGF and provoked

221 EC proliferation, migration, and capillary tube formation in vitro were suppressed more by VEGFR-2

222 ndothelial cell proliferation, migration and tube formation in vitro, and angiogenesis in vivo.

223 cells showed that IGPR-1 regulates capillary tube formation in vitro, and B16F melanoma cells enginee

224 ited EGF receptor signaling, chemotaxis, and tube formation in vitro, and EGF-mediated angiogenesis a

225 -1 administration also increased endothelial tube formation in vitro, which was inhibited by BQ788 or

226 PK signaling in endothelial cells to promote tube formation in vitro.

227 iogenesis as measured by increased capillary tube formation in vitro.

228 TMD1 or Ab against LeY inhibited endothelial tube formation in vitro.

229 onfer enhanced ability to induce endothelial tube formation in vitro.

230 signaling components are required for heart tube formation in zebrafish and that this network modula

231 HLH transcription factor Tal1 in endocardial tube formation: in zebrafish embryos lacking Tal1, endoc

232 g EC is sufficient to induce EC invasion and tube formation, indicating that STAT5A regulates the sec

233 tor promotes the stability of capillary-like tube formation insofar as adding back TGF-beta2 to infec

234 e mice, in vitro three-dimensional capillary tube formation involving HUVEC and/or HTR8 trophoblasts,

235 fraction of CA-SP is present, multi-layered tube formation is blocked, and single-layered tubes pred

236 ancer-induced endothelial cell migration and tube formation, largely by upregulating the expression a

237 onal assays, SsnB inhibited endothelial cell tube formation (Matrigel method) and cell migration (Tra

238 our methods, we have found that subcellular tube formation may proceed through a previously undescri

239 alysis of cellular proliferation, migration, tube formation, microvessel branching, perivascular recr

240 ntly decreased endothelial cell invasion and tube formation more than MK or R5020 treatment alone.

241 via the NRP1-VEGF axis significantly reduced tube formation, new vessel generation and metastasis ind

242 rol VEGF, FSH treatment showed no effects on tube formation, nitric oxide production, wound healing o

243 ration and the migration, proliferation, and tube formation of BMPCs.

244 y enhanced the proliferation, migration, and tube formation of cultured endothelial cells.

245 at RAs promote proliferation, migration, and tube formation of cultured lymphatic endothelial cells b

246 mes secreted in response to hypoxia enhanced tube formation of endothelial cells and decreased profib

247 ed proliferation, migration, transmigration, tube formation of HIMEC, vessel sprouting, and in vivo a

248 ide evidence that PGE2 promotes the in vitro tube formation of human microvascular endothelial cells,

249 in CC cells and that secreted MFAP5 promotes tube formation of human microvascular endothelial cells.

250 y small interfering RNA rescued survival and tube formation of human umbilical vein endothelial cell

251 knockdown cells positively affects vascular tube formation of human umbilical vein endothelial cells

252 expression of MCSF in glioma cells prevented tube formation of human umbilical vein endothelial cells

253 herence, while inhibiting cell migration and tube formation of HUVECs in vitro.

254 Caspase-1 inhibition improves the tube formation of lysophosphatidylcholine-treated HAECs.

255 anslocation in HDMVECs and the migration and tube formation of these cells from inhibition by simvast

256 hether NEU1 might regulate EC capillary-like tube formation on a Matrigel substrate.

257 d on membrane ruffles and protrusions during tube formation on Matrigel.

258 dothelial cell viability, proliferation, and tube formation on Matrigel.

259 ed HMVEC chemotaxis and sJAM-C-induced HMVEC tube formation on Matrigel.

260 RNA clusters with a physiological outcome of tube formation or fibrotic gene expression, partial leas

261 HUVEC migration (P = 0.01) and vessel tube formation (P < 0.01) were significantly increased w

262 Rabconnectin-3 are required for subcellular tube formation, probably in a step resolving the interme

263 The CRHR1 preferred agonist CRH stimulated tube formation, proliferation, and migration of cultured

264 Migration and tube formation properties of brain microvascular endothe

265 Migratory and tube formation properties were enhanced in BMECs from di

266 Here we show that during neural tube formation Rab11-positive recycling endosomes acquir

267 Active VitD (calcitriol) blocked LEC tube formation, reduced LEC proliferation, and induced L

268 ion of the kinase mTOR, regulation of neural tube formation, regulation of cellular hypoxia response,

269 can be uncoupled from outer membrane vesicle/tube formation, reported elsewhere to mediate outer memb

270 use embryos exhibit severe defects in neural tube formation, somitogenesis and cardiac development, h

271 ntivirus expression in assays of endothelial tube formation, sprouting of neovessels from murine aort

272 LEC14A antisera inhibited cell migration and tube formation, suggesting that anti-CLEC14A antibodies

273 -beta and -gamma also stimulated endothelial tube formation to a greater extent than CXCL12-alpha.

274 ic-directed migration as well as endothelial tube formation to persist in in vitro cellular systems,

275 g RNAs rescued ECs from death and stimulated tube formation under stress conditions, confirming the e

276 ssays, IL-32gamma dose-dependently increased tube formation up to 3-fold; an alphaVbeta3 inhibitor pr

277 s achieves gut internalization, linear heart tube formation, ventral body wall closure, and encasemen

278 atory effect on proliferation and angiogenic tube formation via derepression of its direct target gen

279 Migration triggered by VEGF and tube formation was also significantly inhibited by HC.HA

280 ntly increased PI3K/Akt phosphorylation, and tube formation was blocked by treating HUVECs with an Ak

281 In vitro capillary tube formation was inhibited by chNKG2D T cells through

282 nvasion, neurosphere growth, and endothelial tube formation was mitigated by loading miR-1 into gliob

283 S1P-induced in vitro tube formation was significantly attenuated in the prese

284 erize the cellular mechanisms of subcellular tube formation, we have refined methods of high pressure

285 Cell proliferation and tube formation were analyzed, and expression of adhesion

286 HRMEC proliferation and tube formation were assayed according to standard protoc

287 s and their paracrine effects on endothelial tube formation were increased after exposure to IH in vi

288 and EC-CFU paracrine effects on endothelial tube formation were significantly higher in AMI-SDB comp

289 SSc-conditioned media inhibited EC tube formation, whereas addition of vitamin E, by reduci

290 hibits cell migration and in vitro capillary tube formation, whereas co-knockdown of PML compromises

291 as PKA-activatable substrates, inhibits the tube formation, whereas knockdown of RhoA or glycogen sy

292 lls, TRPC1, TRPC4, and STIM1 are involved in tube formation, whereas Orai1 has no effect.

293 lly active WT NEU1 dose-dependently impaired tube formation, whereas overexpression of either a catal

294 avin in control of microvascular endothelial tube formation, wherein gravin functions as a "braking"

295 6 and sIL-6R promoted angiogenic endothelial tube formation, which could be blocked by silencing SP4.

296 ical vein endothelial cell proliferation and tube formation, which was blocked by the MEK inhibitor,

297 rRNA gene transcription, proliferation, and tube formation, which were inhibited by blocking ANG nuc

298 pG2-stimulated HUVEC migration, adhesion and tube formation; which may be due to its inhibition on ST

299 -1 ECs inhibits migration, proliferation and tube formation, with p27 accumulation being responsible

300 formation is a critical event in biological tube formation, yet its molecular mechanisms remain poor