ライフサイエンスコーパス: vascular endothelial growth factor

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

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

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

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

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

6 epithelial phenotype was enhanced following vascular endothelial growth factor A (VEGF-A) exposure.

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

8 Vascular endothelial growth factor A (VEGF-A) produced l

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

10 helial cell migration, and tube formation in vascular endothelial growth factor A (VEGF-A) stimulated

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

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

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

14 d new blood vessel sprouts is coordinated by vascular endothelial growth factor A (VEGFA) and Delta-l

15 a-induced factor 1a (Hif1a) and secretion of vascular endothelial growth factor A (Vegfa) by starved

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

17 Vascular endothelial growth factor a (Vegfa) is essentia

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

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

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

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

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

23 ptors present in dermal fibroblasts restores vascular endothelial growth factor A production by these

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

25 ally impaired and produce reduced amounts of vascular endothelial growth factor A, resulting in defic

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

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

28 Vascular endothelial growth factor-A (VEGF-A) acts via 2

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

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

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

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

33 Leishmania major increases the expression of vascular endothelial growth factor-A and vascular endoth

34 Vascular endothelial growth factor-A mRNA and protein ex

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

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

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

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

39 Anti-vascular endothelial growth factor agents are proposed a

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

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

42 Comparisons of the relative effect of 3 anti-vascular endothelial growth factor agents to treat diabe

43 ssociated with treatment using biologic anti-vascular endothelial growth factor agents.

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

45 Vascular endothelial growth factor-amniotic fluid stem c

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

47 Vascular endothelial growth factor-amniotic fluid stem c

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

49 Cxcl9 produced by osteoblasts interacts with vascular endothelial growth factor and prevents its bind

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

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

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

53 [growth-regulated protein alpha], and VEGF [vascular endothelial growth factor]), and an increase in

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

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

56 d clinical trial (RCT) evaluating the 3 anti-vascular endothelial growth factor (anti-VEGF) agents af

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

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

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

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

61 7028), retinal OCT imaging (92134), and anti-vascular endothelial growth factor (anti-VEGF) treatment

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

63 Treatments included anti-vascular endothelial growth factors (anti-VEGFs), steroi

64 on diabetic macular oedema [DMO] after anti-vascular endothelial growth factor [anti-VEGF] treatment

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

66 ith the combination of anti-miR-630 and anti-vascular endothelial growth factor antibody in mice resu

67 We considered that vascular endothelial growth factor-B (VEGF-B), which pro

68 Vascular endothelial growth factor C (Vegfc) activates i

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

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

71 flammation resulted in reduced expression of vascular endothelial growth factor-C and decreased corne

72 gulated the expression of prolymphangiogenic vascular endothelial growth factor-C upon stimulation wi

73 lial cells, isolated HKMECs depended on high vascular endothelial growth factor concentration for sur

74 el permeability and elevated blood levels of vascular endothelial growth factor D and stromal cell-de

75 recommendations for sirolimus treatment and vascular endothelial growth factor D testing and recomme

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

77 future comparative efficacy studies of anti-vascular endothelial growth factor drugs for DME.

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

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

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

81 Vascular endothelial growth factor has emerged as a sign

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

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

84 evelopment and angiogenesis, but its role in vascular endothelial growth factor-induced endothelial c

85 tamate transporter on astrocytes through the vascular endothelial growth factor inducing favorable ch

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

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

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

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

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

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

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

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

94 transforming growth factors beta1 and beta2, vascular endothelial growth factor, interleukin-1beta, m

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

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

97 treatment was associated with decreased free vascular endothelial growth factor (not bound to bevaciz

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

99 Sunitinib, a vascular endothelial growth factor pathway inhibitor, is

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

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

102 blood supply might upregulate production of vascular endothelial growth factor, providing the stimul

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

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

105 tions from vascular tumors were stained with vascular endothelial growth factor receptor (VEGFR), vas

106 of vascular endothelial growth factor-A and vascular endothelial growth factor receptor (VEGFR)-2 an

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

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

109 th factor receptor 2 antibody) or icrucumab (vascular endothelial growth factor receptor 1 antibody)

110 nolase, placental growth factor, and soluble vascular endothelial growth factor receptor 1 levels wer

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

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

113 Vascular endothelial growth factor receptor 2 (VEGFR2) l

114 as a new class of potent and selective human vascular endothelial growth factor receptor 2 (VEGFR2) t

115 ptide, based on an amyloidogenic fragment of vascular endothelial growth factor receptor 2 (VEGFR2),

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

117 r docetaxel in combination with ramucirumab (vascular endothelial growth factor receptor 2 antibody)

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

119 4, alpha-smooth muscle actin, CD31, phospho-vascular endothelial growth factor receptor 2, and p42/4

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

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

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

123 Vascular endothelial growth factor receptor 3 (VEGFR3) i

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

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

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

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

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

129 endothelial growth factor receptor (VEGFR), vascular endothelial growth factor receptor type 1 (VEGF

130 study, the possible localization and role of vascular endothelial growth factor receptor type 2 (VEGF

131 lial growth factor receptor type 1 (VEGFR1), vascular endothelial growth factor receptor type 2 (VEGF

132 growth factor receptor type 2 (VEGFR2), and vascular endothelial growth factor receptor type 3 (VEGF

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

134 Novel PET imaging agents for assessing vascular endothelial growth factor receptor-2 (VEGFR-2)

135 rs for the receptor tyrosine kinases MET and Vascular Endothelial Growth factor Receptor-2 (VEGFR-2).

136 4 and subsets coexpressing CD133, CXCR4, and vascular endothelial growth factor receptor-2 epitopes.

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

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

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

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

141 67, vascular endothelial growth factors A/C, vascular endothelial growth factor receptors 2/3, angiop

142 years, tyrosine kinase inhibitors targeting vascular endothelial growth factor receptors and RET (re

143 s an inhibitor of kinases, including MET and vascular endothelial growth factor receptors, and has sh

144 othelial growth factor-A (VEGF-A) acts via 2 vascular endothelial growth factor receptors, VEGFR-1 an

145 glucose consumption, lactate production and vascular endothelial growth factor secretion.

146 pg/mL, P<0.001) and significantly decreased vascular endothelial growth factor/sFlt1 ratio (P=0.012)

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

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

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

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

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

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

153 Our data provide rationale for combining vascular endothelial growth factor-targeting therapy wit

154 tic macular edema (DME) after months of anti-vascular endothelial growth factor therapy and its effec

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

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

157 nforms the debate regarding the role of anti-vascular endothelial growth factor therapy in patients w

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

159 opathy complexes are less responsive to anti-vascular endothelial growth factor therapy with no prosp

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

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

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

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

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

165 umab treatment, suggesting that earlier anti-vascular endothelial growth factor treatment of center-i

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

167 thresholds of CST for trials evaluating anti-vascular endothelial growth factor treatments.

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

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

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

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

172 provide additional outcomes comparing 3 anti-vascular endothelial growth factor (VEGF) agents for DME

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

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

175 anibizumab are the most frequently used anti-vascular endothelial growth factor (VEGF) agents injecte

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

177 thesis and investigate concentrations of: 1) vascular endothelial growth factor (VEGF) and 2) platele

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

179 Vascular endothelial growth factor (VEGF) and glial fibr

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

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

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

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

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

185 ies, we show that TTF-1 positively regulates vascular endothelial growth factor (VEGF) and that the V

186 Biologics targeting vascular endothelial growth factor (VEGF) are the major

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

188 texts, Reck impacts vascular biology via the vascular endothelial growth factor (VEGF) cascade.

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

190 Renin and vascular endothelial growth factor (VEGF) contents in CD

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

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

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

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

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

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

197 By basic fibroblast growth factor (bFGF) or vascular endothelial growth factor (VEGF) gene therapy v

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

199 ich is paralleled by increased expression of vascular endothelial growth factor (VEGF) in macrophages

200 Vascular endothelial growth factor (VEGF) induces angiog

201 hat affects some, but not all, recipients of vascular endothelial growth factor (VEGF) inhibitors giv

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

203 re used to identify the total number of anti-vascular endothelial growth factor (VEGF) injections adm

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

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

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

207 Vascular endothelial growth factor (VEGF) is a powerful

208 Vascular endothelial growth factor (VEGF) is implicated

209 th platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) is increased d

210 migration of the developing forebrain, while vascular endothelial growth factor (VEGF) is known to in

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

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

213 The vascular endothelial growth factor (VEGF) isoform VEGF16

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

215 Vascular endothelial growth factor (VEGF) level was high

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

217 Anti-vascular endothelial growth factor (VEGF) medicines have

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

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

220 pes through randomised trials, incorporating vascular endothelial growth factor (VEGF) pathway inhibi

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

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

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

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

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

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

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

228 Capillaries express vascular endothelial growth factor (VEGF) receptors, inc

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

230 Vascular endothelial growth factor (VEGF) regulates angi

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

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

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

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

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

236 project, the redundancy between endoglin and vascular endothelial growth factor (VEGF) signaling in a

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

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

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

240 In previous studies, we showed that renal vascular endothelial growth factor (VEGF) therapy attenu

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

242 Anti-vascular endothelial growth factor (VEGF) therapy is com

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

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

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

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

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

248 cular degeneration (nAMD) for different anti-vascular endothelial growth factor (VEGF) treatment sche

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

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

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

252 erformed for hepatocyte growth factor (HGF), vascular endothelial growth factor (VEGF), and c-Met rec

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

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

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

256 The isolation of vascular endothelial growth factor (VEGF), characterizat

257 elevated pAkt activation and expressions of vascular endothelial growth factor (VEGF), Flk1, and VE-

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

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

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

261 host hepatocyte, but not tumour cell-derived vascular endothelial growth factor (VEGF), is responsibl

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

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

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

265 s, which migrate in response to gradients of vascular endothelial growth factor (VEGF), stalk cells,

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

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

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

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

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

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

272 We show that ECS cell-produced vascular endothelial growth factor (VEGF)-A is required

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

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

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

276 s of GSH-protein adducts, capillary density, vascular endothelial growth factor (VEGF)-A, and HIF-1al

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

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

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

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

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

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

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

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

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

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

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

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

289 f connective tissue growth factor (CTGF) and vascular endothelial growth factor (VEGF).

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

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

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

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

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

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

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

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

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

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

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