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

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

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

3 ibitor of metalloproteinases 1, and vascular endothelial growth factor.

4 Genome wide studies indicate that vascular endothelial growth factor A (VEGF) is associated with os

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

6 al 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 locally is

9 OINTS: Progressive depletion of all vascular endothelial growth factor A (VEGF-A) splice isoforms fro

10 ll migration, and tube formation in vascular endothelial growth factor A (VEGF-A) stimulated HREC cul

11 ncipal effectors of vasculogenesis, vascular endothelial growth factor A (VEGF-A), and platelet-deriv

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

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

14 od vessel sprouts is coordinated by vascular endothelial growth factor A (VEGFA) and Delta-like ligan

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

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

17 Vascular endothelial growth factor a (Vegfa) is essential for blo

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

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

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

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

22 of the proangiogenic growth factor vascular endothelial growth factor A and promoted the proliferati

23 sent in dermal fibroblasts restores vascular endothelial growth factor A production by these cells, r

24 tidylinositol 3-kinase and inhibits vascular endothelial growth factor A secretion by tumor cells, in

25 ired and produce reduced amounts of vascular endothelial growth factor A, resulting in deficient angi

26 liferation and angiogenesis (Ki-67, vascular endothelial growth factors A/C, vascular endothelial gro

27 nhibited Akt and p38 stimulation by vascular endothelial growth factor, a major driver of angiogenesi

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

29 th one of its main natural ligands, vascular endothelial growth factor-A (VEGF-A), contributing to ne

30 neurotrophic growth factor (BDNF), vascular endothelial growth factor-A (VEGF-A), insulin-like growt

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

32 5 x 10(12) viral particles encoding vascular endothelial growth factor-A [VEGF-A] or thymosin beta 4

33 a major increases the expression of vascular endothelial growth factor-A and vascular endothelial gro

34 Vascular endothelial growth factor-A mRNA and protein expression

35 Vascular endothelial growth factor-A, VEGF-C, and VEGF-R2 mRNA ex

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

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

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

39 Anti-vascular endothelial growth factor agents are proposed as treatme

40 aluate the effect of switching anti-vascular endothelial growth factor agents for treatment of neovas

41 aluate the effect of switching anti-vascular endothelial growth factor agents for treatment of neovas

42 ns of the relative effect of 3 anti-vascular endothelial growth factor agents to treat diabetic macul

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

44 Vascular endothelial growth factor-amniotic fluid stem cells can

45 injury, amniotic fluid stem cells, vascular endothelial growth factor-amniotic fluid stem cells in t

46 groups: amniotic fluid stem cells, vascular endothelial growth factor-amniotic fluid stem cells in t

47 Vascular endothelial growth factor-amniotic fluid stem cells indu

48 e, an agent that inhibits both anti-vascular endothelial growth factor and anti-platelet-derived grow

49 duced by osteoblasts interacts with vascular endothelial growth factor and prevents its binding to EC

50 ansdifferentiation formulation that included endothelial growth factors and innate immune activator p

51 eceptor-associated tyrosine kinase, vascular endothelial growth factor, and cell cycle pathways, wher

52 reased CCA histidine decarboxylase, vascular endothelial growth factor, and MC/EMT/ECM expression tha

53 factors (fibroblast growth factor, vascular endothelial growth factor, and platelet-derived growth f

54 n angiogenic pathways such as VEGF (vascular endothelial growth factor), ANG1 (angiopoietin 1), ANG2

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

56 l trial (RCT) evaluating the 3 anti-vascular endothelial growth factor (anti-VEGF) agents aflibercept

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

58 was primarily driven by use of anti-vascular endothelial growth factor (anti-VEGF) injections from 20

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

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

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

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

63 Treatments included anti-vascular endothelial growth factors (anti-VEGFs), steroids, and p

64 tic macular oedema [DMO] after anti-vascular endothelial growth factor [anti-VEGF] treatment.

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

66 ombination of anti-miR-630 and anti-vascular endothelial growth factor antibody in mice resulted in r

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

68 Vascular endothelial growth factor C (Vegfc) activates its recept

69 Lymphatic development promoting vascular endothelial growth factor C (VEGFC) is associated with p

70 ing EGF-like growth factor (HBEGF), vascular endothelial growth factor C (VEGFC), betacellulin (BTC),

71 n resulted in reduced expression of vascular endothelial growth factor-C and decreased corneal lympha

72 he expression of prolymphangiogenic vascular endothelial growth factor-C upon stimulation with IL-10.

73 s, isolated HKMECs depended on high vascular endothelial growth factor concentration for survival and

74 bility and elevated blood levels of vascular endothelial growth factor D and stromal cell-derived fac

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

76 pathophysiological role of impaired vascular endothelial growth factor-dependent vascular remodeling.

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

78 or, platelet-derived growth factor, vascular endothelial growth factor), endothelin and inhibitors of

79 Up-regulation of vascular endothelial growth factor enhances the therapeutic effec

80 RB with increased vascular leakage, vascular endothelial growth factor expression, and infiltrating m

81 Vascular endothelial growth factor has emerged as a significant c

82 vels and mesenchymal cells, but not vascular endothelial growth factor in Hyal2(-/-) embryonic hearts

83 rosine kinase 2 (ERBB2 or HER2), or vascular endothelial growth factor, including trastuzumab, ramuci

84 t and angiogenesis, but its role in vascular endothelial growth factor-induced endothelial cell (EC)

85 ansporter on astrocytes through the vascular endothelial growth factor inducing favorable changes in

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

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

88 t experiences specific to receiving vascular endothelial growth factor inhibitors (anti-VEGF) for wet

89 raised that intravitreal dosing of vascular endothelial growth factor inhibitors in DME could be ass

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

91 Subsequently, anti-vascular endothelial growth factor injections and panretinal phot

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

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

94 ing growth factors beta1 and beta2, vascular endothelial growth factor, interleukin-1beta, matrix met

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

96 K)](2) PET/CT correlated with serum vascular endothelial growth factor levels, whereas baseline lung/

97 evacizumab is a frequently used antivascular endothelial growth factor medication in the United State

98 was associated with decreased free vascular endothelial growth factor (not bound to bevacizumab) and

99 ing intravitreal injections of anti-vascular endothelial growth factor or verteporfin photodynamic th

100 Sunitinib, a vascular endothelial growth factor pathway inhibitor, is an effec

101 rosis factor-alpha (TNF-alpha), and vascular endothelial growth factor peaked on day 6 (P </=0.05) an

102 The HIF target vascular endothelial growth factor promoted ATII cell proliferati

103 pply might upregulate production of vascular endothelial growth factor, providing the stimulus for ne

104 Angiogenesis, in which vascular endothelial growth factor receptor (VEGFR) 2 plays an es

105 al multikinase inhibitors targeting vascular endothelial growth factor receptor (VEGFR) and approved

106 m vascular tumors were stained with vascular endothelial growth factor receptor (VEGFR), vascular end

107 lar endothelial growth factor-A and vascular endothelial growth factor receptor (VEGFR)-2 and is asso

108 hes, we show that the expression of vascular endothelial growth factor receptor 1 (VEGFR1) by pericyt

109 CXCR7 expression and recruitment of vascular endothelial growth factor receptor 1 (VEGFR1)-expressing

110 receptor 2 antibody) or icrucumab (vascular endothelial growth factor receptor 1 antibody) after pro

111 lacental growth factor, and soluble vascular endothelial growth factor receptor 1 levels were poor pr

112 rmation (evidenced by a decrease in vascular endothelial growth factor receptor 1 positive (VEGFR1(+)

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

114 Vascular endothelial growth factor receptor 2 (VEGFR2) localized

115 sed on an amyloidogenic fragment of vascular endothelial growth factor receptor 2 (VEGFR2), a protein

116 graphy (US) by using clinical-grade vascular endothelial growth factor receptor 2 (VEGFR2)-targeted m

117 el in combination with ramucirumab (vascular endothelial growth factor receptor 2 antibody) or icrucu

118 dothelial nitric oxide synthase/Akt/vascular endothelial growth factor receptor 2 signaling, and a re

119 he combination of anti-TLR2 and antivascular endothelial growth factor receptor 2 yielded an additive

120 -smooth muscle actin, CD31, phospho-vascular endothelial growth factor receptor 2, and p42/44 mitogen

121 inib is an oral potent inhibitor of vascular endothelial growth factor receptor 2, MET, and AXL and i

122 dothelial nitric oxide synthase/Akt/vascular endothelial growth factor receptor 2/oxidative stress-in

123 is by monoclonal antibodies against vascular endothelial growth factor receptor 3 (VEGFR-3) ameliorat

124 Vascular endothelial growth factor receptor 3 (VEGFR3) is an attr

125 helial cell adhesion molecule 1 and vascular endothelial growth factor receptor 3 (VEGFR3).

126 rs (prospero homeobox protein 1 and vascular endothelial growth factor receptor 3) as well as blood e

127 se each of plastic microspheres and vascular endothelial growth factor receptor antagonist in polysty

128 SF1) with the combined treatment of vascular endothelial growth factor receptor blocker SU5416.

129 othelial growth factor signaling by vascular endothelial growth factor receptor inhibition may comple

130 racting protein-1 prevented 20-HETE-mediated endothelial growth factor receptor phosphorylation and a

131 ial growth factor receptor (VEGFR), vascular endothelial growth factor receptor type 1 (VEGFR1), vasc

132 e possible localization and role of vascular endothelial growth factor receptor type 2 (VEGFR2) in th

133 th factor receptor type 1 (VEGFR1), vascular endothelial growth factor receptor type 2 (VEGFR2), and

134 actor receptor type 2 (VEGFR2), and vascular endothelial growth factor receptor type 3 (VEGFR3).

135 Membrane-localized vascular endothelial growth factor receptor-1 (mVEGFR1) is an end

136 el PET imaging agents for assessing vascular endothelial growth factor receptor-2 (VEGFR-2) expressio

137 e receptor tyrosine kinases MET and Vascular Endothelial Growth factor Receptor-2 (VEGFR-2).

138 sets coexpressing CD133, CXCR4, and vascular endothelial growth factor receptor-2 epitopes.

139 clear cells expressing CD34, CD133, vascular endothelial growth factor receptor-2, and chemokine (C-X

140 sis and lymphangiogenesis involving vascular endothelial growth factor-receptor tyrosine kinase and T

141 isting of PECAM-1, VE-cadherin, and vascular endothelial growth factor receptors (VEGFRs) that reside

142 ine kinase activity associated with vascular endothelial growth factor receptors 1, 2, and 3, current

143 lar endothelial growth factors A/C, vascular endothelial growth factor receptors 2/3, angiopoietin 1/

144 bitor of kinases, including MET and vascular endothelial growth factor receptors, and has shown activ

145 growth factor-A (VEGF-A) acts via 2 vascular endothelial growth factor receptors, VEGFR-1 and VEGFR-2

146 consumption, lactate production and vascular endothelial growth factor secretion.

147 <0.001) and significantly decreased vascular endothelial growth factor/sFlt1 ratio (P=0.012) compared

148 e and SF, as they may interact with vascular endothelial growth factor signaling and exRNA.

149 SP1 fragment, suppresses heightened vascular endothelial growth factor signaling and preserves BMEC t

150 olymerase inhibition and/or reduced vascular endothelial growth factor signaling by vascular endothel

151 ting hypoxia inducible factor (HIF)/vascular endothelial growth factor signaling, are initially effec

152 To evaluate if the up-regulation of vascular endothelial growth factor strengthens the protective eff

153 aches, including the use of soluble vascular endothelial growth factor (sVEGF)-VEGF165, have been dev

154 Participants who received antivascular endothelial growth factor therapies for neovascular AMD

155 ar edema (DME) after months of anti-vascular endothelial growth factor therapy and its effect on visu

156 t treatment options, including anti-vascular endothelial growth factor therapy and laser retinal phot

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

158 e debate regarding the role of anti-vascular endothelial growth factor therapy in patients with PDR w

159 Although anti-vascular endothelial growth factor therapy requires a more freque

160 mplexes are less responsive to anti-vascular endothelial growth factor therapy with no prospective cl

161 of visual loss sustained with anti-vascular endothelial growth factor therapy, and have the potentia

162 oximates that of intravitreous anti-vascular endothelial growth factor therapy.

163 interleukin-6, interleukin-10, and vascular endothelial growth factor to the medium.

164 festyles and implementation of anti-vascular endothelial growth factor treatment are the most likely

165 The advent of anti-vascular endothelial growth factor treatment has changed the prog

166 tment, suggesting that earlier anti-vascular endothelial growth factor treatment of center-involving

167 fter 2006 were calculated since antivascular endothelial growth factor treatment was introduced natio

168 primarily aimed at optimizing anti-vascular endothelial growth factor treatments that have the poten

169 s of CST for trials evaluating anti-vascular endothelial growth factor treatments.

170 very of the growth factors bFGF and vascular endothelial growth factor using a mineral coated surgica

171 up II: 0.11 (0.11) ng/mL, P = .01); vascular endothelial growth factor (VEGF) (Group I: 157.0 (154.0)

172 stered in combination with the anti-vascular endothelial growth factor (VEGF) agent ranibizumab (Luce

173 Intravitreous injections of anti-vascular endothelial growth factor (VEGF) agents are associated w

174 dditional outcomes comparing 3 anti-vascular endothelial growth factor (VEGF) agents for DME.

175 ocular safety and efficacy of anti-vascular endothelial growth factor (VEGF) agents for the treatmen

176 The introduction of anti-vascular endothelial growth factor (VEGF) agents has stimulated c

177 b are the most frequently used anti-vascular endothelial growth factor (VEGF) agents injected intravi

178 ravitreal injections (IVTs) of anti-vascular endothelial growth factor (VEGF) agents.

179 d investigate concentrations of: 1) vascular endothelial growth factor (VEGF) and 2) platelet-derived

180 asts by enhancing the activities of vascular endothelial growth factor (VEGF) and fibroblast growth f

181 Vascular endothelial growth factor (VEGF) and glial fibrillary ac

182 evaluated epigenetic modulation of vascular endothelial growth factor (VEGF) and hypoxia-inducible f

183 S-treated CLI muscle expressed more vascular endothelial growth factor (VEGF) and interleukin-10 (IL-

184 iation of chondrocytes by promoting vascular endothelial growth factor (VEGF) and matrix metalloprote

185 ine kinase inhibitor active against vascular endothelial growth factor (VEGF) and platelet-derived gr

186 nsor that can simultaneously detect vascular endothelial growth factor (VEGF) and prostate-specific a

187 how that TTF-1 positively regulates vascular endothelial growth factor (VEGF) and that the VEGF promo

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

189 Vascular endothelial growth factor (VEGF) B belongs to the VEGF f

190 ck impacts vascular biology via the vascular endothelial growth factor (VEGF) cascade.

191 B-9778 combined with suppression of vascular endothelial growth factor (VEGF) causes a significantly

192 Renin and vascular endothelial growth factor (VEGF) contents in CD were eva

193 alling in liver buds, and show that vascular endothelial growth factor (VEGF) crosstalk potentiates e

194 n (nAMD) treated with a single anti-vascular endothelial growth factor (VEGF) drug monotherapy for 1

195 atment of ischemic diseases.Soluble vascular endothelial growth factor (VEGF) enhances vascular engra

196 or microvascular density (MVD), and vascular endothelial growth factor (VEGF) expression) from 9 pati

197 nd BDNF-I transcripts and increased vascular endothelial growth factor (VEGF) expression.

198 Members of vascular endothelial growth factor (VEGF) family are overexpresse

199 To characterize the expression of vascular endothelial growth factor (VEGF) in a patient with retin

200 ralleled by increased expression of vascular endothelial growth factor (VEGF) in macrophages at the B

201 Vascular endothelial growth factor (VEGF) induces angiogenesis an

202 ts some, but not all, recipients of vascular endothelial growth factor (VEGF) inhibitors given as par

203 nd after intravitreal injections of vascular endothelial growth factor (VEGF) inhibitors.

204 o identify the total number of anti-vascular endothelial growth factor (VEGF) injections administered

205 Three patients underwent anti-vascular endothelial growth factor (VEGF) intravitreal injections

206 Targeting vascular endothelial growth factor (VEGF) is a common treatment s

207 Vascular endothelial growth factor (VEGF) is a major driver of bl

208 Vascular endothelial growth factor (VEGF) is a powerful regulator

209 Vascular endothelial growth factor (VEGF) is implicated in the pe

210 et-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) is increased during the

211 of the developing forebrain, while vascular endothelial growth factor (VEGF) is known to influence r

212 KEY POINTS: Peripheral vascular endothelial growth factor (VEGF) is necessary for exerci

213 RATIONALE: Vascular endothelial growth factor (VEGF) is the main driver of a

214 The vascular endothelial growth factor (VEGF) isoform VEGF165 stimula

215 al diseases (PAD) by increasing the vascular endothelial growth factor (VEGF) level in endothelial ce

216 Vascular endothelial growth factor (VEGF) level was highly co-sta

217 first 10 years of intravitreal anti-vascular endothelial growth factor (VEGF) medication use for opht

218 Anti-vascular endothelial growth factor (VEGF) medicines have revoluti

219 y cleaves, the AP for activation of vascular endothelial growth factor (VEGF) or endonuclease III-lik

220 This phenomenon requires vascular endothelial growth factor (VEGF) originating from outsid

221 gh randomised trials, incorporating vascular endothelial growth factor (VEGF) pathway inhibitors into

222 marily through dysregulation of the vascular endothelial growth factor (VEGF) pathway.

223 Therapies targeting oncologic and vascular endothelial growth factor (VEGF) pathways have failed to

224 in 10 articles that addressed anti-vascular endothelial growth factor (VEGF) pharmacotherapies for M

225 ed the influence of this pathway on vascular endothelial growth factor (VEGF) production and tumour v

226 a3/alpha5beta1 scaffolds delivering vascular endothelial growth factor (VEGF) promoted non-tortuous b

227 as a negative feedback regulator of vascular endothelial growth factor (VEGF) receptor activation.

228 ABSTRACT: Signalling through vascular endothelial growth factor (VEGF) receptors and the tyros

229 Capillaries express vascular endothelial growth factor (VEGF) receptors, including ne

230 that tivozanib, a pan-inhibitor of vascular endothelial growth factor (VEGF) receptors, inhibited pr

231 Vascular endothelial growth factor (VEGF) regulates angiogenesis,

232 We also show how vascular endothelial growth factor (VEGF) regulates PRKCB promote

233 Because deficiency of vascular endothelial growth factor (VEGF) results in thrombotic m

234 rther demonstrate the importance of Vascular Endothelial Growth Factor (VEGF) secretion for this path

235 receptor 1 (CX3CR1) expression and vascular endothelial growth factor (VEGF) secretion in Mos/Mps by

236 al pathways activated downstream of vascular endothelial growth factor (VEGF) signaling during angiog

237 the redundancy between endoglin and vascular endothelial growth factor (VEGF) signaling in angiogenes

238 ling transducers and isoforms along vascular endothelial growth factor (VEGF) signaling pathways at c

239 Here, we showed that vascular endothelial growth factor (VEGF) signaling within the gl

240 teriolargenesis requires endogenous vascular endothelial growth factor (VEGF) signalling.

241 vious studies, we showed that renal vascular endothelial growth factor (VEGF) therapy attenuated MV d

242 Anti-vascular endothelial growth factor (VEGF) therapy has demonstrate

243 Anti-vascular endothelial growth factor (VEGF) therapy is commonly use

244 comes in RVO eyes treated with anti-vascular endothelial growth factor (VEGF) therapy may provide inf

245 patients on pro re nata (PRN) anti-vascular endothelial growth factor (VEGF) therapy with >1 year fo

246 ng CXCR4 with POL5551 disrupts anti-vascular endothelial growth factor (VEGF) therapy-induced glioma

247 r degeneration (AMD) receiving anti-vascular endothelial growth factor (VEGF) therapy.

248 (hepatocytes), which then produces vascular endothelial growth factor (VEGF) to enable the subsequen

249 eneration (nAMD) for different anti-vascular endothelial growth factor (VEGF) treatment schemes.

250 lar degeneration (nAMD) during anti-vascular endothelial growth factor (VEGF) treatment.

251 l growth factor receptor (EGFR) and vascular endothelial growth factor (VEGF) were targeted with anti

252 e-guanine, is robustly inhibited by vascular endothelial growth factor (VEGF), a previously identifie

253 for hepatocyte growth factor (HGF), vascular endothelial growth factor (VEGF), and c-Met receptor exp

254 f pro-angiogenic factors, CXCL1 and vascular endothelial growth factor (VEGF), and reduced CD31(+) bl

255 oluble signaling factors, including vascular endothelial growth factor (VEGF), and that CAFs generate

256 However, low plasma levels of vascular endothelial growth factor (VEGF), but high levels of thr

257 The isolation of vascular endothelial growth factor (VEGF), characterization of it

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

259 n of pro-angiogenic signals such as vascular endothelial growth factor (VEGF), hypoxia also stimulate

260 cell-derived factor 1 (SDF-1alpha), vascular endothelial growth factor (VEGF), hypoxia-inducible fact

261 lementation decreased the levels of vascular endothelial growth factor (VEGF), inducible nitric oxide

262 tocyte, but not tumour cell-derived vascular endothelial growth factor (VEGF), is responsible for can

263 esis, including the potent promoter vascular endothelial growth factor (VEGF), is therefore an attrac

264 (R)), a monoclonal antibody against vascular endothelial growth factor (VEGF), is used clinically to

265 otein 10, interleukin (IL)-6, IL-8, vascular endothelial growth factor (VEGF), monocyte chemoattracti

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

267 Protein drugs that neutralize vascular endothelial growth factor (VEGF), such as aflibercept or

268 ndogenous growth factors, including vascular endothelial growth factor (VEGF), that normally stimulat

269 The levels of 6 cytokines-vascular endothelial growth factor (VEGF), tumor necrosis factor

270 A model drug, vascular endothelial growth factor (VEGF), was encapsulated in RD

271 ed matrices increased production of vascular endothelial growth factor (VEGF), while matrices display

272 Vascular endothelial growth factor (VEGF)-A has been implicated i

273 r premiR-150 transfection increased vascular endothelial growth factor (VEGF)-A mRNA and secretion in

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

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

276 protein adducts, capillary density, vascular endothelial growth factor (VEGF)-A, and HIF-1alpha in th

277 ell proliferation by regulating the vascular endothelial growth factor (VEGF)-A, VEGF-C, FGFR3, and p

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

279 ls, von Willebrand factor (vWF) and vascular endothelial growth factor (VEGF)-C expression were measu

280 xycycline-induced overexpression of vascular endothelial growth factor (VEGF)-C was driven by the adi

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

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

283 n pancreatic tumor endothelium in a vascular endothelial growth factor (VEGF)-independent manner.

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

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

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

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

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

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

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

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

292 eriodontal diseases, supported with vascular endothelial growth factor (VEGF-A) and tumor necrosis fa

293 and CRP), cell adhesion molecules (VCAM-1), endothelial growth factors (VEGF) and VDBP.

294 lymer NPs with nM affinity to a key vascular endothelial growth factor (VEGF165) inhibit binding of t

295 Vascular endothelial growth factor (VEGFA), a pivotal regulator o

296 ells where it was shown to modulate vascular endothelial growth factor (VEGFR)-2 and epidermal growth

297 f classic vasoactive factors (e.g., vascular endothelial growth factor) were similar in ERM patients

298 its a substantial increase of VEGF (vascular endothelial growth factor), which mediates the regulatio

299 mas, inhibition with bevacizumab of vascular endothelial growth factor, which is an important stimulu

300 ated at tyrosine 731 in response to vascular endothelial growth factor, which likely contributes to h

301 ly down-regulated the expression of vascular endothelial growth factor while increasing that of pigme