ライフサイエンスコーパス: tube formation

1 growing bundles as a dynamical bottleneck to tube formation.

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

3 laments, significantly delaying bundling and tube formation.

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

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

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

7 U inhibited cellular invasion, migration and tube formation.

8 lmonary endothelial adhesion, migration, and tube formation.

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

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

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

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

13 in angiogenic complexes and EC sprouting and tube formation.

14 ew new colonies could develop following germ tube formation.

15 counteracted NEU1-mediated inhibition of EC tube formation.

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

17 -2 induced EC marker expression and in vitro tube formation.

18 ding proliferation, migration, and capillary tube formation.

19 s upregulates PECAM1 expression and promotes tube formation.

20 regulates vasculogenesis through endothelial tube formation.

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

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

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

24 -93 overexpression enhanced endothelial cell tube formation.

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

26 significant and dose-responsive increase in tube formation.

27 -AP also inhibited endothelial migration and tube formation.

28 VEGF-induced endothelial cell migration and tube formation.

29 ributed to endothelial cell infiltration and tube formation.

30 kdown impairs endothelial cell migration and tube formation.

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

32 f vascular permeability and endothelial cell tube formation.

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

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

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

36 educed chemotherapy-induced endothelial cell tube formation.

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

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

39 ls to restore endothelial cell sprouting and tube formation.

40 increased endothelial cell proliferation and tube formation.

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

42 anisotropic partition of lipids, leading to tube formation.

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

44 ndothelial cell proliferation, migration, or tube formation.

45 ed proliferation but increased migration and tube formation.

46 cell proliferation, migration, and capillary tube formation.

47 sed endothelial proliferation, migration and tube formation.

48 reduced HRMEC migration, proliferation, and tube formation.

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

50 ed to increased migration, proliferation and tube formation.

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

52 and also induced endothelial cell capillary tube formation.

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

54 isms involved in folate action during neural tube formation.

55 odulation of HRMVEC migration, sprouting and tube formation.

56 impaired endothelial cell proliferation and tube formation.

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

58 lial cells from apoptosis and restored their tube formation.

59 tic events including gastrulation and neural tube formation.

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

61 othelial cells induced apoptosis and blocked tube formation.

62 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)

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

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

65 tion of miR-548aq-3p was correlated with the tube formation activity of CAD ECFCs enhanced by FIR.

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

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

68 dothelial cell proliferation, migration, and tube formation, along with reduced VEGFR3, Akt, and endo

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

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

71 etal lung endothelial cell proliferation and tube formation and alveolar type 2 cell proliferation we

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

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

74 The effect of MC(TC)s on in vitro tube formation and barrier function was studied using pr

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

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

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

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

79 miR-214-3p in endothelial cells reduced the tube formation and cell migration.

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

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

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

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

84 escent endothelial cells experience impaired tube formation and delayed wound healing.

85 Developmental genetics of corolla tube formation and elaboration 697 VI.

86 patterns, developmental genetics of corolla tube formation and elaboration, and the molecular basis

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

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

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

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

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

92 , endothelial progenitor cell migration, and tube formation and inhibited osteoclast formation, migra

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

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

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

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

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

98 idative stress-related pathway, and impaired tube formation and migration, confirming endothelial dys

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

100 testican-2 increased glomerular endothelial tube formation and motility, raising the possibility tha

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 r domain of BafA induces cell proliferation, tube formation and sprouting of microvessels, and drives

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

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

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

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

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

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

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

113 oreover, while HIF-1alpha inhibition reduced tube formation and wound healing closure, microRNA-126 l

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

130 ssion inhibits cell migration, invasion, and tube formation, and this suppressive effect was relieved

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

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

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

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

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

136 ces, including proliferation, migration, and tube formation, are all significantly reduced in hCAECs

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

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

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

140 Moreover, the endothelial tube formation assay revealed significant morphological

141 , the most commonly used is the "Endothelial Tube Formation Assay" (ETFA).

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

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

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

145 ype rescue experiments using the endothelial tube formations assay, (2) training the algorithm to ide

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

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

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

149 analysis and endothelial cell chemotaxis and tube formation assays.

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

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

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

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

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

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

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

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

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

159 ress-induced impairment in proliferation and tube formation by HUVECs.

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

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

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

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

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

165 n of ORP2 from ECs inhibits their angiogenic tube formation capacity, alters the gene expression of a

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 DED directly promoted VEC proliferation and tube formation compared with normal controls.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

188 Moreover, HE4 promoted increases in tube formation in an in vitro model of angiogenesis, whi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

205 ted EC proliferation, migration, and network tube formation in matrigel, whereas miR-135-3p neutraliz

206 hanges in cell migration, proliferation, and tube formation in Matrigel.

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

208 dothelial cell proliferation, migration, and tube formation in response to palmitic acid, and a poten

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

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

211 s VEGF-induced proliferation, migration, and tube formation in vitro and angiogenesis in vivo.

212 oliferation, migration, and endothelial cell tube formation in vitro and breast tumor growth, angioge

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

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

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

224 cells (HLECs) to promote HLECs migration and tube formation in vitro, and facilitate lymphangiogenesi

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

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

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

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

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

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

231 001 muM to 1 muM) increased endothelial cell tube formation indicating enhanced angiogenesis.

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

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

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

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

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

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

245 48aq-3p contributes to the inhibition of the tube formation of ECFCs.

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

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

250 -overexpressing breast cancer cells promoted tube formation of human umbilical vein endothelial cells

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

252 knockdown cells positively affects vascular 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 RNA clusters with a physiological outcome of tube formation or fibrotic gene expression, partial leas

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

260 significantly in NI cells (p < 0.001), where tube formation (p < 0.05) was also improved.

261 dothelial cells, promoting proliferation and tube formation, possibly through protein kinase B, extra

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

263 Migration and tube formation properties of brain microvascular endothe

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

265 Chemical genetic screening of endothelial tube formation provides a robust approach for identifyin

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

267 reading, attachment, migration, and in vitro tube formation rates of S315A variant-overexpressing cel

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

269 investigated, the intervening process of gut tube formation remains relatively understudied(7,8).

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

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

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

273 th siRNA lead to reduced eNOS expression and tube formation suggesting the involvement of CCR10 in EC

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

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

276 nvolved in cell proliferation, migration and tube formation, triggered by the angiogenesis inducers V

277 ced in vitro migration (transwell assay) and tube formation (tube length) capacities in a subpopulati

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

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

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

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

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

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

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

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

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

287 p < 0.001), and defects in wound closure and tube formation were apparent in NP ECFCs (p < 0.01).

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

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

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

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

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

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

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

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

296 6 and sIL-6R promoted angiogenic endothelial tube formation, which could be blocked by silencing SP4.

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

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