ライフサイエンスコーパス: vascular endothelial

1 In human primary vascular endothelial and smooth muscle cells that endoge

2 ttributed to the effects of hyperglycemia on vascular endothelial and smooth muscle cells, but the un

3 l p120-catenin (p120) maintains the level of vascular endothelial cadherin (VE-Cad) by inhibiting VE-

4 modelling of adherens contacts consisting of vascular endothelial cadherin (VE-cadherin) and beta-cat

5 lines expressing either SNAP-tagged Notch or vascular endothelial cadherin (VE-cadherin), we provide

6 phorylation of the adherens junction protein vascular endothelial cadherin (VEC).

7 function is impaired and the localization of vascular endothelial cadherin is altered as function of

8 Consistent with elevated VEGFR2 activity, vascular endothelial cadherin showed reduced localizatio

9 ial-specific adherens junction protein, VEC (vascular endothelial cadherin), upregulate genes with ke

10 complex in the plasma membrane consisting of vascular endothelial cadherin, the transmembrane protein

11 co-localized and co-immunoprecipitated with vascular endothelial cadherin-based complexes, including

12 t such as junctional adhesion molecule-1 and vascular endothelial cadherin.

13 ockout (LKB1(endo-/-)) mice by crossbreeding vascular endothelial-cadherin-Cre mice with LKB1(flox/fl

14 s of TrpRS by enhancing its interaction with vascular endothelial-cadherin.

15 We show here that vascular endothelial cell (EC)-specific reduction in Rec

16 Vascular endothelial cell dysfunction mediated by antiph

17 reatly hindered by barriers presented by the vascular endothelial cell layer and by the aberrant natu

18 MDBA after acute ascorbic acid infusion, and vascular endothelial cell protein expression of NADPH ox

19 functions ascribed in its interactions with vascular endothelial cells (EC), including migration and

20 nner, for the proliferation and migration of vascular endothelial cells (ECs) during retinal angiogen

21 Transplanting vascular endothelial cells (ECs) to support metabolism a

22 se BRB disintegration, it sensitizes retinal vascular endothelial cells (ECs) to VEGF-A, leading to u

23 Infantile hemangiomas are benign tumors of vascular endothelial cells (ECs), characterized by three

24 ogenes (SpCas9) is used to deplete VEGFR2 in vascular endothelial cells (ECs), whereby the expression

25 , GSC also transdifferentiate into bona fide vascular endothelial cells (GEC), which inherit mutation

26 and wound-healing activity of PGE2 in human vascular endothelial cells (HUVECs) although the amount

27 ytotoxicity test of the Mg extract via human vascular endothelial cells (HUVECs) indicates that the c

28 T cells were either cocultured with vascular endothelial cells (VECs) to assess VEC prolifer

29 Upon their activation and firm adhesion to vascular endothelial cells (VECs), leukocytes preferenti

30 BLB, there were numerous vesicles within the vascular endothelial cells (VECs), with increased number

31 g its nuclear receptor in cardiomyocytes and vascular endothelial cells and by regulating the renin-a

32 hese cells are induced to differentiate into vascular endothelial cells and cardiomyocytes possibly b

33 on of galectin-3 with unknown receptor(s) on vascular endothelial cells and causes endothelial secret

34 romotes the angiogenesis and the invasion of vascular endothelial cells and fibroblasts by enhancing

35 sic shear stress responses commonly in blood vascular endothelial cells and LECs.

36 om dermal blood and lymphatic vessels (blood vascular endothelial cells and lymphatic endothelial cel

37 covering the point of contact between donor vascular endothelial cells and the recipient's immune ce

38 hus plays a critical role in the behavior of vascular endothelial cells by inhibiting migration.

39 sed no obvious changes, specific deletion in vascular endothelial cells caused CNV and a phenotype si

40 Recently, cross-talk between GSC and vascular endothelial cells has been shown to significant

41 cytotoxic T cells, is generally expressed in vascular endothelial cells in healthy human tissues.

42 Short-term deletion of Vegfr3 in blood vascular endothelial cells increased baseline leakage in

43 r 1 (RUNX1) as a gene upregulated in CD31(+) vascular endothelial cells obtained from human PDR fibro

44 in the normal human utricular stroma showed vascular endothelial cells with few pinocytotic vesicles

45 channels are also thought to be expressed in vascular endothelial cells, but their presence and funct

46 for cis-regulatory elements, particularly in vascular endothelial cells, consistent with a primary ro

47 ly lack ET-1 in hematopoietic stem cells and vascular endothelial cells, did not produce ET-1 even wh

48 Endothelin 1 (ET-1), mainly produced from vascular endothelial cells, induces vasoconstriction in

49 mpJX-594 initially infected tumor vascular endothelial cells, leading to vascular pruning

50 y activity in quiescent and angiogenic blood vascular endothelial cells, thereby preventing excessive

51 oxidant that induces oxidative stress on the vascular endothelial cells, thus mediating progression o

52 tain a reduced number of resident intraislet vascular endothelial cells.

53 tudied canonical interactions identified for vascular endothelial cells.

54 rs, and beta-catenin-dependent signalling in vascular endothelial cells.

55 r pericytes, enwrapping and associating with vascular endothelial cells.

56 ates independent of the production system in vascular endothelial cells.

57 increased ferritin immunolabeling in retinal vascular endothelial cells.

58 pression of Slco2a1 in the tumour-associated vascular endothelial cells.

59 ial cells and corneal keratocytes as well as vascular endothelial cells.

60 IL-1beta, TNF-alpha, and IL-10 secretion in vascular endothelial cells.

61 CD144/VE-cadherin, and CD106/Endoglin, from vascular endothelial cells.

62 in/+) mice with loss of insulin receptors in vascular endothelial cells.

63 l types, including microglia, astrocytes and vascular endothelial cells.

64 Vascular endothelial dysfunction and increased arterial

65 reticulum (ER) stress has been implicated in vascular endothelial dysfunction of obesity, diabetes, a

66 for vascular ER stress and ER stress-induced vascular endothelial dysfunction, and that miR-204 promo

67 Gut microbiota promotes atherosclerosis, and vascular endothelial dysfunction, signalled by impaired

68 protected from diabetic oxidative stress and vascular endothelial dysfunction.

69 miR-204 protects against tunicamycin-induced vascular/endothelial ER stress, associated impairment of

70 We measured vascular endothelial function by brachial artery flow-me

71 of prostaglandin A2 (PGA2) in modulation of vascular endothelial function is unknown.

72 hip between sympathetic nervous activity and vascular endothelial function.

73 The splice isoforms of vascular endothelial growth A (VEGF) each have different

74 To analyze anti-vascular endothelial growth factor (anti-VEGF) agent-ass

75 Anti-vascular endothelial growth factor (anti-VEGF) drugs can

76 ologists was primarily driven by use of anti-vascular endothelial growth factor (anti-VEGF) injection

77 Anti-vascular endothelial growth factor (anti-VEGF) therapy f

78 ipants had been treated previously with anti-vascular endothelial growth factor (anti-VEGF) therapy,

79 7028), retinal OCT imaging (92134), and anti-vascular endothelial growth factor (anti-VEGF) treatment

80 ral approaches, including the use of soluble vascular endothelial growth factor (sVEGF)-VEGF165, have

81 g/mL, Group II: 0.11 (0.11) ng/mL, P = .01); vascular endothelial growth factor (VEGF) (Group I: 157.

82 t, administered in combination with the anti-vascular endothelial growth factor (VEGF) agent ranibizu

83 Intravitreous injections of anti-vascular endothelial growth factor (VEGF) agents are ass

84 ce on the ocular safety and efficacy of anti-vascular endothelial growth factor (VEGF) agents for the

85 The introduction of anti-vascular endothelial growth factor (VEGF) agents has sti

86 after intravitreal injections (IVTs) of anti-vascular endothelial growth factor (VEGF) agents.

87 d fibroblasts by enhancing the activities of vascular endothelial growth factor (VEGF) and fibroblast

88 Vascular endothelial growth factor (VEGF) and glial fibr

89 e I trial evaluated epigenetic modulation of vascular endothelial growth factor (VEGF) and hypoxia-in

90 ng to pFUS-treated CLI muscle expressed more vascular endothelial growth factor (VEGF) and interleuki

91 differentiation of chondrocytes by promoting vascular endothelial growth factor (VEGF) and matrix met

92 ral tyrosine kinase inhibitor active against vascular endothelial growth factor (VEGF) and platelet-d

93 ity biosensor that can simultaneously detect vascular endothelial growth factor (VEGF) and prostate-s

94 Vascular endothelial growth factor (VEGF) B belongs to t

95 ons of AKB-9778 combined with suppression of vascular endothelial growth factor (VEGF) causes a signi

96 gate signalling in liver buds, and show that vascular endothelial growth factor (VEGF) crosstalk pote

97 generation (nAMD) treated with a single anti-vascular endothelial growth factor (VEGF) drug monothera

98 r the treatment of ischemic diseases.Soluble vascular endothelial growth factor (VEGF) enhances vascu

99 ures, tumor microvascular density (MVD), and vascular endothelial growth factor (VEGF) expression) fr

100 BDNF-IV and BDNF-I transcripts and increased vascular endothelial growth factor (VEGF) expression.

101 Members of vascular endothelial growth factor (VEGF) family are ove

102 To characterize the expression of vascular endothelial growth factor (VEGF) in a patient w

103 Vascular endothelial growth factor (VEGF) induces angiog

104 before and after intravitreal injections of vascular endothelial growth factor (VEGF) inhibitors.

105 Three patients underwent anti-vascular endothelial growth factor (VEGF) intravitreal i

106 Targeting vascular endothelial growth factor (VEGF) is a common tr

107 Vascular endothelial growth factor (VEGF) is a major dri

108 Vascular endothelial growth factor (VEGF) is a powerful

109 Vascular endothelial growth factor (VEGF) is implicated

110 KEY POINTS: Peripheral vascular endothelial growth factor (VEGF) is necessary f

111 RATIONALE: Vascular endothelial growth factor (VEGF) is the main dr

112 The vascular endothelial growth factor (VEGF) isoform VEGF16

113 al arterial diseases (PAD) by increasing the vascular endothelial growth factor (VEGF) level in endot

114 Vascular endothelial growth factor (VEGF) level was high

115 rize the first 10 years of intravitreal anti-vascular endothelial growth factor (VEGF) medication use

116 fficiently cleaves, the AP for activation of vascular endothelial growth factor (VEGF) or endonucleas

117 This phenomenon requires vascular endothelial growth factor (VEGF) originating fr

118 rates primarily through dysregulation of the vascular endothelial growth factor (VEGF) pathway.

119 Therapies targeting oncologic and vascular endothelial growth factor (VEGF) pathways have

120 dentified in 10 articles that addressed anti-vascular endothelial growth factor (VEGF) pharmacotherap

121 nvestigated the influence of this pathway on vascular endothelial growth factor (VEGF) production and

122 ivo, alpha3/alpha5beta1 scaffolds delivering vascular endothelial growth factor (VEGF) promoted non-t

123 of CCN1 as a negative feedback regulator of vascular endothelial growth factor (VEGF) receptor activ

124 ABSTRACT: Signalling through vascular endothelial growth factor (VEGF) receptors and

125 e we show that tivozanib, a pan-inhibitor of vascular endothelial growth factor (VEGF) receptors, inh

126 Vascular endothelial growth factor (VEGF) regulates angi

127 We also show how vascular endothelial growth factor (VEGF) regulates PRKC

128 Because deficiency of vascular endothelial growth factor (VEGF) results in thr

129 r data further demonstrate the importance of Vascular Endothelial Growth Factor (VEGF) secretion for

130 chemokine receptor 1 (CX3CR1) expression and vascular endothelial growth factor (VEGF) secretion in M

131 scriptional pathways activated downstream of vascular endothelial growth factor (VEGF) signaling duri

132 ous signaling transducers and isoforms along vascular endothelial growth factor (VEGF) signaling path

133 Here, we showed that vascular endothelial growth factor (VEGF) signaling with

134 diated arteriolargenesis requires endogenous vascular endothelial growth factor (VEGF) signalling.

135 Anti-vascular endothelial growth factor (VEGF) therapy has de

136 etter outcomes in RVO eyes treated with anti-vascular endothelial growth factor (VEGF) therapy may pr

137 PCV patients on pro re nata (PRN) anti-vascular endothelial growth factor (VEGF) therapy with >

138 ntagonizing CXCR4 with POL5551 disrupts anti-vascular endothelial growth factor (VEGF) therapy-induce

139 ed macular degeneration (AMD) receiving anti-vascular endothelial growth factor (VEGF) therapy.

140 arenchyme (hepatocytes), which then produces vascular endothelial growth factor (VEGF) to enable the

141 ated macular degeneration (nAMD) during anti-vascular endothelial growth factor (VEGF) treatment.

142 epidermal growth factor receptor (EGFR) and vascular endothelial growth factor (VEGF) were targeted

143 -phosphate-guanine, is robustly inhibited by vascular endothelial growth factor (VEGF), a previously

144 duction of pro-angiogenic factors, CXCL1 and vascular endothelial growth factor (VEGF), and reduced C

145 nhanced soluble signaling factors, including vascular endothelial growth factor (VEGF), and that CAFs

146 However, low plasma levels of vascular endothelial growth factor (VEGF), but high leve

147 production of pro-angiogenic signals such as vascular endothelial growth factor (VEGF), hypoxia also

148 stromal cell-derived factor 1 (SDF-1alpha), vascular endothelial growth factor (VEGF), hypoxia-induc

149 ion, supplementation decreased the levels of vascular endothelial growth factor (VEGF), inducible nit

150 angiogenesis, including the potent promoter vascular endothelial growth factor (VEGF), is therefore

151 (Avastin(R)), a monoclonal antibody against vascular endothelial growth factor (VEGF), is used clini

152 ucible protein 10, interleukin (IL)-6, IL-8, vascular endothelial growth factor (VEGF), monocyte chem

153 Protein drugs that neutralize vascular endothelial growth factor (VEGF), such as aflib

154 vels of endogenous growth factors, including vascular endothelial growth factor (VEGF), that normally

155 The levels of 6 cytokines-vascular endothelial growth factor (VEGF), tumor necrosi

156 A model drug, vascular endothelial growth factor (VEGF), was encapsula

157 HA-enriched matrices increased production of vascular endothelial growth factor (VEGF), while matrice

158 Vascular endothelial growth factor (VEGF)-A has been imp

159 ing EVs or premiR-150 transfection increased vascular endothelial growth factor (VEGF)-A mRNA and sec

160 Alternate splicing in the exon-8 of vascular endothelial growth factor (VEGF)-A results in p

161 Messenger RNA (mRNA) expression of vascular endothelial growth factor (VEGF)-A, -C, and VEG

162 nhanced cell proliferation by regulating the vascular endothelial growth factor (VEGF)-A, VEGF-C, FGF

163 their heterogeneous vasculature by secreting vascular endothelial growth factor (VEGF)-A.

164 cular cells, von Willebrand factor (vWF) and vascular endothelial growth factor (VEGF)-C expression w

165 where doxycycline-induced overexpression of vascular endothelial growth factor (VEGF)-C was driven b

166 Vascular endothelial growth factor (VEGF)-D is capable o

167 Although much is known about vascular endothelial growth factor (VEGF)-dependent regu

168 pressed on pancreatic tumor endothelium in a vascular endothelial growth factor (VEGF)-independent ma

169 LSD1 cooperates with CBP and MTA1 to enhance vascular endothelial growth factor (VEGF)-induced tumor

170 For example, vascular endothelial growth factor (VEGF)-mediated angio

171 Long-term intraocular injections of vascular endothelial growth factor (VEGF)-neutralising p

172 its receptors in the PT to alter splicing of vascular endothelial growth factor (VEGF).

173 hrough a hypoxia induced upregulation of the vascular endothelial growth factor (VEGF).

174 tude and duration of angiogenesis induced by vascular endothelial growth factor (VEGF).

175 Moreover, the splicing profile of vascular endothelial growth factor (VEGF)165/VEGF165b tr

176 esis of periodontal diseases, supported with vascular endothelial growth factor (VEGF-A) and tumor ne

177 Polymer NPs with nM affinity to a key vascular endothelial growth factor (VEGF165) inhibit bin

178 Vascular endothelial growth factor (VEGFA), a pivotal re

179 cancer cells where it was shown to modulate vascular endothelial growth factor (VEGFR)-2 and epiderm

180 Genome wide studies indicate that vascular endothelial growth factor A (VEGF) is associate

181 ges were characterized by high expression of vascular endothelial growth factor A (VEGF).

182 Everolimus inhibits vascular endothelial growth factor A (VEGF-A) expression

183 KEY POINTS: Progressive depletion of all vascular endothelial growth factor A (VEGF-A) splice iso

184 f two principal effectors of vasculogenesis, vascular endothelial growth factor A (VEGF-A), and plate

185 (for example, carbonic anhydrase 9 (CA9) and vascular endothelial growth factor A (VEGF-A).

186 ociated with a decrease in the expression of vascular endothelial growth factor A (VEGF-A).

187 Vascular endothelial growth factor A (VEGFA) is a key fa

188 Vascular endothelial growth factor a (Vegfa) is essentia

189 dr expression to enable the DH to respond to vascular endothelial growth factor A (VEGFA) ligand from

190 IL-6 activated the STAT3/vascular endothelial growth factor A (VEGFA) pathway dir

191 deletion of hypoxia-response element in the vascular endothelial growth factor A (VEGFA) promoter sh

192 h factor AA and BB; placental growth factor; vascular endothelial growth factor A and D; vascular end

193 abundance of the proangiogenic growth factor vascular endothelial growth factor A and promoted the pr

194 d phosphatidylinositol 3-kinase and inhibits vascular endothelial growth factor A secretion by tumor

195 ar edema does not respond to an initial anti-vascular endothelial growth factor agent, usually after

196 ophthalmologists may switch to another anti-vascular endothelial growth factor agent.

197 Anti-vascular endothelial growth factor agents are proposed a

198 oup to evaluate the effect of switching anti-vascular endothelial growth factor agents for treatment

199 oup to evaluate the effect of switching anti-vascular endothelial growth factor agents for treatment

200 nib malate, an agent that inhibits both anti-vascular endothelial growth factor and anti-platelet-der

201 Inadequate tumor uptake of the vascular endothelial growth factor antibody bevacizumab

202 Lymphatic development promoting vascular endothelial growth factor C (VEGFC) is associat

203 arin-binding EGF-like growth factor (HBEGF), vascular endothelial growth factor C (VEGFC), betacellul

204 Up-regulation of vascular endothelial growth factor enhances the therapeu

205 of the BRB with increased vascular leakage, vascular endothelial growth factor expression, and infil

206 Vascular endothelial growth factor has emerged as a sign

207 sed HA levels and mesenchymal cells, but not vascular endothelial growth factor in Hyal2(-/-) embryon

208 First-line treatment with a vascular endothelial growth factor inhibitor remains the

209 g one or more prior regimens that included a vascular endothelial growth factor inhibitor.

210 ed patient experiences specific to receiving vascular endothelial growth factor inhibitors (anti-VEGF

211 have been raised that intravitreal dosing of vascular endothelial growth factor inhibitors in DME cou

212 In eyes treated with vascular endothelial growth factor inhibitors, vascular

213 Subsequently, anti-vascular endothelial growth factor injections and panret

214 amount of intervention requiring 1 or 2 anti-vascular endothelial growth factor injections only.

215 Treatment with intravitreous anti-vascular endothelial growth factor injections resulted i

216 l levels along with inappropriate attenuated vascular endothelial growth factor levels may imply an a

217 E-[c(RGDfK)](2) PET/CT correlated with serum vascular endothelial growth factor levels, whereas basel

218 es including intravitreal injections of anti-vascular endothelial growth factor or verteporfin photod

219 tumor necrosis factor-alpha (TNF-alpha), and vascular endothelial growth factor peaked on day 6 (P </

220 The HIF target vascular endothelial growth factor promoted ATII cell pr

221 Angiogenesis, in which vascular endothelial growth factor receptor (VEGFR) 2 pl

222 ib are oral multikinase inhibitors targeting vascular endothelial growth factor receptor (VEGFR) and

223 l approaches, we show that the expression of vascular endothelial growth factor receptor 1 (VEGFR1) b

224 ssion of CXCR7 expression and recruitment of vascular endothelial growth factor receptor 1 (VEGFR1)-e

225 niche formation (evidenced by a decrease in vascular endothelial growth factor receptor 1 positive (

226 vascular endothelial growth factor A and D; vascular endothelial growth factor receptor 1, 2, and 3;

227 Vascular endothelial growth factor receptor 2 (VEGFR2) l

228 ultrasonography (US) by using clinical-grade vascular endothelial growth factor receptor 2 (VEGFR2)-t

229 nsity, endothelial nitric oxide synthase/Akt/vascular endothelial growth factor receptor 2 signaling,

230 4, alpha-smooth muscle actin, CD31, phospho-vascular endothelial growth factor receptor 2, and p42/4

231 Cabozantinib is an oral potent inhibitor of vascular endothelial growth factor receptor 2, MET, and

232 by an endothelial nitric oxide synthase/Akt/vascular endothelial growth factor receptor 2/oxidative

233 ngiogenesis by monoclonal antibodies against vascular endothelial growth factor receptor 3 (VEGFR-3)

234 Vascular endothelial growth factor receptor 3 (VEGFR3) i

235 let/endothelial cell adhesion molecule 1 and vascular endothelial growth factor receptor 3 (VEGFR3).

236 tic markers (prospero homeobox protein 1 and vascular endothelial growth factor receptor 3) as well a

237 single dose each of plastic microspheres and vascular endothelial growth factor receptor antagonist i

238 (obese ZSF1) with the combined treatment of vascular endothelial growth factor receptor blocker SU54

239 cular endothelial growth factor signaling by vascular endothelial growth factor receptor inhibition m

240 Membrane-localized vascular endothelial growth factor receptor-1 (mVEGFR1)

241 od mononuclear cells expressing CD34, CD133, vascular endothelial growth factor receptor-2, and chemo

242 plex consisting of PECAM-1, VE-cadherin, and vascular endothelial growth factor receptors (VEGFRs) th

243 of tyrosine kinase activity associated with vascular endothelial growth factor receptors 1, 2, and 3

244 67, vascular endothelial growth factors A/C, vascular endothelial growth factor receptors 2/3, angiop

245 ial tissue and SF, as they may interact with vascular endothelial growth factor signaling and exRNA.

246 iogenic TSP1 fragment, suppresses heightened vascular endothelial growth factor signaling and preserv

247 ribose) polymerase inhibition and/or reduced vascular endothelial growth factor signaling by vascular

248 se abrogating hypoxia inducible factor (HIF)/vascular endothelial growth factor signaling, are initia

249 To evaluate if the up-regulation of vascular endothelial growth factor strengthens the prote

250 Current treatment options, including anti-vascular endothelial growth factor therapy and laser ret

251 Information on the effect of anti-vascular endothelial growth factor therapy in eyes with

252 Although anti-vascular endothelial growth factor therapy requires a mo

253 he amount of visual loss sustained with anti-vascular endothelial growth factor therapy, and have the

254 rate approximates that of intravitreous anti-vascular endothelial growth factor therapy.

255 retion of interleukin-6, interleukin-10, and vascular endothelial growth factor to the medium.

256 lthier lifestyles and implementation of anti-vascular endothelial growth factor treatment are the mos

257 The advent of anti-vascular endothelial growth factor treatment has changed

258 nvAMD are primarily aimed at optimizing anti-vascular endothelial growth factor treatments that have

259 Delivery of the growth factors bFGF and vascular endothelial growth factor using a mineral coate

260 gnificantly down-regulated the expression of vascular endothelial growth factor while increasing that

261 rations of classic vasoactive factors (e.g., vascular endothelial growth factor) were similar in ERM

262 nvolved in angiogenic pathways such as VEGF (vascular endothelial growth factor), ANG1 (angiopoietin

263 owth factor, platelet-derived growth factor, vascular endothelial growth factor), endothelin and inhi

264 tion elicits a substantial increase of VEGF (vascular endothelial growth factor), which mediates the

265 us also inhibited Akt and p38 stimulation by vascular endothelial growth factor, a major driver of an

266 ctivate receptor-associated tyrosine kinase, vascular endothelial growth factor, and cell cycle pathw

267 luids increased CCA histidine decarboxylase, vascular endothelial growth factor, and MC/EMT/ECM expre

268 iogenesis factors (fibroblast growth factor, vascular endothelial growth factor, and platelet-derived

269 ceptor tyrosine kinase 2 (ERBB2 or HER2), or vascular endothelial growth factor, including trastuzuma

270 nant gliomas, inhibition with bevacizumab of vascular endothelial growth factor, which is an importan

271 hosphorylated at tyrosine 731 in response to vascular endothelial growth factor, which likely contrib

272 action with one of its main natural ligands, vascular endothelial growth factor-A (VEGF-A), contribut

273 n derived neurotrophic growth factor (BDNF), vascular endothelial growth factor-A (VEGF-A), insulin-l

274 The effects of vascular endothelial growth factor-A (VEGF-A/VEGF) and i

275 (rAAV) (5 x 10(12) viral particles encoding vascular endothelial growth factor-A [VEGF-A] or thymosi

276 Vascular endothelial growth factor-A mRNA and protein ex

277 Vascular endothelial growth factor-A, VEGF-C, and VEGF-R

278 athway, activating HIF-target genes, notably vascular endothelial growth factor-A.

279 perfusion injury, amniotic fluid stem cells, vascular endothelial growth factor-amniotic fluid stem c

280 Vascular endothelial growth factor-amniotic fluid stem c

281 d to four groups: amniotic fluid stem cells, vascular endothelial growth factor-amniotic fluid stem c

282 Vascular endothelial growth factor-amniotic fluid stem c

283 pivotal pathophysiological role of impaired vascular endothelial growth factor-dependent vascular re

284 angiogenesis and lymphangiogenesis involving vascular endothelial growth factor-receptor tyrosine kin

285 migration of LSK cells in response to SDF or vascular endothelial growth factor.

286 ta, arginase-1, matrix metalloproteinase and vascular endothelial growth factor.

287 issue inhibitor of metalloproteinases 1, and vascular endothelial growth factor.

288 cular degeneration (NVAMD) treated with anti-vascular endothelial growth factors (anti-VEGF).

289 rs of proliferation and angiogenesis (Ki-67, vascular endothelial growth factors A/C, vascular endoth

290 r endothelium are known to lead to increased vascular endothelial leak, but the underlying molecular

291 RATIONALE: Vascular endothelial mitochondrial dysfunction contribut

292 duce more oxidants at birth suggest that the vascular endothelial mitochondrial dysfunction seen at b

293 vascular stabilization including claudin-5, vascular endothelial-protein tyrosine phosphatase (VE-PT

294 granuloma-induced vascular permeability via vascular endothelial-protein tyrosine phosphatase inhibi

295 The role of vascular endothelial (VE) components in dengue infection

296 the interaction and requirement of IL-4 and vascular endothelial (VE) IL-4 receptor alpha chain (IL-

297 eam kinase signaling to the barrier effector vascular endothelial (VE)-cadherin and induced vascular

298 of Wnt7b led to greatly diminished levels of vascular endothelial (VE)-cadherin at the cell surface i

299 Vascular endothelial (VE)-cadherin plays a critical role

300 Vascular endothelial (VE)-cadherin undergoes constitutiv