ライフサイエンスコーパス: VEGF

1 VEGF also changes expression of genes that are known to

2 VEGF concentrations correlated with central subfield thi

3 VEGF quickly relaxes the endothelial cell barrier by tri

4 VEGF-A was a potent inducer of glycolysis in tubulogenic

5 VEGF-C not only can serve as a diagnostic biomarker but

6 VEGFs and Ang1 participate in the pathophysiology of U-H

7 gingival crevicular fluid (GCF) HIF-1alpha, VEGF, and TNF-alpha levels in generalized aggressive per

8 all clinical parameters and GCF HIF-1alpha, VEGF, and TNF-alpha levels were significantly higher in

9 newly identified TR4/lincRNA-p21/HIF-1alpha/VEGF-A signaling with Bex, an FDA-approved drug, may inc

10 ia modulating the TR4/lincRNA-p21/HIF-1alpha/VEGF-A signaling.

11 Western blot measurements of HIF-1a, HIF-2a, VEGF (vascular endothelial growth factor), and eNOS (end

12 very of BMP2 and soluble VEGFR1 (sVEGFR1), a VEGF receptor antagonist, in a hydrogel skewed different

13 uch as vascular endothelial growth factor A (VEGF).

14 Vascular endothelial growth factor A (VEGF-A) and its binding to VEGFRs is an important angiog

15 campal vascular endothelial growth factor-A (VEGF-A) in both male and female mice, as well as increas

16 nodes, vascular endothelial growth factor-A (VEGF-A), vascular endothelial growth factor-C (VEGF-C) w

17 ia the vascular endothelial growth factor-A (VEGF-A)/VEGF receptor 2 (VEGFR2) pathway.

18 ascular endothelial growth factor-A (VEGF-A)/VEGF receptor 2 (VEGFR2) pathway.

19 0 fg/mL for DSG3, and 0.20 fg/mL for VEGF-A, VEGF-C and beta-Tub.

20 We found a significant increase of VEGF-A, VEGF-C, and Ang1 levels in U-HAE patients compared to co

21 upregulation of pro(lymph)angiogenic VEGF-A, VEGF-C, VEGF-D and infiltration of macrophages.

22 AAV8-VEGF-C injection significantly increased meningeal lymph

23 8-vascular endothelial growth factor C (AAV8-VEGF-C) was injected into the cisterna magna of HE rats

24 Furthermore, AAV8-VEGF-C decreased microglia activation (P < .001) and neu

25 inly according to their mechanism of action: VEGF inhibitors or anti-angiogenic agents, EGFR inhibito

26 t perturb Wnt signaling but rather activates VEGF.

27 spectively, and validated the known affinity VEGF-A(121):VEGFR2 as K(D) = 0.66 nM.

28 changes were seen in each compartment after VEGF inhibition, including genes involved in migration,

29 Although VEGF (vascular endothelial growth factor) improves lung

30 by 8 hours post-mTBI, particularly GAS-1 and VEGF-B were increased while CXCL16 reduced, 23 proteins

31 measured binding kinetics for VEGFA(165) and VEGF-A(121), but binding kinetics of the other two pro-

32 and its downstream effectors HIF-1alpha and VEGF-A in cell lines, xenografts, and transgenic murine

33 t in increasing the expression of VEGF-A and VEGF-C via targeting the 3'UTR of mRNAs at a post-transc

34 cular endothelial growth factor (VEGF)-C and VEGF-D.

35 oxygen responsive target genes (eg, EPO and VEGF), certain members of the oxygen/2-oxoglutarate-depe

36 on and proliferation whereas both GW0742 and VEGF-A promoted tubulogenesis.

37 Dual blockade of PD-L1 and VEGF has enhanced anticancer immunity through multiple m

38 ein claudin-5 were increased with norrin and VEGF or with VEGF alone, but both norrin and VEGF were r

39 VEGF or with VEGF alone, but both norrin and VEGF were required for enriched claudin-5 localization a

40 n affinities between VEGF-A(165a):VEGFR1 and VEGF-A(165a):VEGFR2, 1.0 pM and 10 pM respectively, and

41 (165), -A(165b), and -A(121) with VEGFR1 and VEGF-R2 using surface plasmon resonance.

42 leading cause of vision loss worldwide, and VEGF inhibitors are the primary treatment for nAMD.

43 During angiogenesis, VEGF acts as an attractive cue for endothelial cells (EC

44 ificant upregulation of pro(lymph)angiogenic VEGF-A, VEGF-C, VEGF-D and infiltration of macrophages.

45 Anti-VEGF agents are efficient treatment to maintain visual a

46 Anti-VEGF gene therapy approaches can create significantly di

47 Anti-VEGF injection rates and treatment switches were not imp

48 Anti-VEGF-naive eyes diagnosed with nAMD that commenced treat

49 /317) of study eyes received at least 1 anti-VEGF treatment (median, 4; interquartile range [IQR], 0-

50 ween groups (laser [20/635 eyes], 3.1%; anti-VEGF [1/74 eyes], 1.4%; P = 0.27).

51 s, received a mean of 6.0 (range, 1-27) anti-VEGF injections, and underwent 7.2 OCT and 5.3 FA examin

52 ields the best cost utility among the 3 anti-VEGF agents modeled.

53 At 1 year, after a mean of 7.3 anti-VEGF injections, there was a mean gain of 1 letter (0.95

54 1%) of 13 patients received 1.3 +/- 0.6 anti-VEGF injections.

55 ated with poor treatment response after anti-VEGF injections.

56 therapy (29/368 eyes [7.9%]) than after anti-VEGF therapy (0/90 eyes [0%]; P < 0.001).

57 mic serious adverse events (SAEs) after anti-VEGF treatment have been low.

58 to identify effectors by which VEGF and anti-VEGF control the endothelial cell barrier in cells that

59 o identify baseline characteristics and anti-VEGF treatment details.

60 influenced both barrier relaxation and anti-VEGF-mediated closure.

61 ls less than 4 weeks are used to assess anti-VEGF treatment response.

62 ed predefined systemic outcomes between anti-VEGF agents occurring within 180 days of treatment initi

63 1) alone and combined with bevacizumab (anti-VEGF) in patients with unresectable hepatocellular carci

64 h nonexudative AMD but is unaffected by anti-VEGF treatments, suggesting a retinal vascular contribut

65 in gene expression were not reversed by anti-VEGF.

66 ative systemic safety profile of common anti-VEGF agents remains incompletely understood.

67 Ten patients (91%) received concurrent anti-VEGF injections at the time of tube erosion, and the ave

68 In contrast, for PCV eyes, anti-VEGF monotherapy and combination therapy with PDT yielde

69 nti-vascular endothelial growth factor (anti-VEGF) treatments or geographic atrophy (GA).

70 (25.5% vs. 13.2%; P = 0.014), and fewer anti-VEGF injections (7.6 vs. 10.2; P = 0.001).

71 erval between FAc implant and the first anti-VEGF had a significant linear positive relationship with

72 expenditures and patient copayments for anti-VEGF agents with increasing reimbursement and use of bev

73 Age, gender, anti-VEGF treatment type, number of treatments, and VA were e

74 single, relatively short-term lapse in anti-VEGF treatment in patients with DME did not appear to re

75 an unintended minimum 3-month lapse in anti-VEGF treatment, with a control group of DME patients rec

76 rtheast showed lower odds of initiating anti-VEGF treatment (OR = 0.60; 95%CI, 0.44-0.82; P < 0.001)

77 Our results suggest intravitreal anti-VEGF injections are linked to higher rates of recurrent

78 Intravitreal anti-VEGF naive patients seen between 2010 and 2019 of White

79 tly seen in eyes receiving intravitreal anti-VEGF therapy for type 1 MNV due to AMD.

80 lusion criteria were prior intravitreal anti-VEGF treatment, invasive ophthalmologic interventions, a

81 ation of 0.58 kDa rhodamine and 153 kDa anti-VEGF monoclonal antibody (bevacizumab) upon IA injection

82 an 16 weeks have elapsed since the last anti-VEGF injection.

83 -time alternative treatment to lifelong anti-VEGF treatment for nAMD.

84 date in nAMD, identified relatively low anti-VEGF injection frequencies, coupled with moderate anatom

85 o present minimal toxicity and maintain anti-VEGF potency, suggesting that our approach may have the

86 years of therapy in eyes requiring more anti-VEGF injections; however, we cannot exclude that the RNF

87 The faster action of anti-VEGF agents likely is responsible for these findings.

88 more likely to occur within 30 days of anti-VEGF injection than after 30 days.

89 ts experienced an SMH within 30 days of anti-VEGF injection.

90 Self-reports of anti-VEGF injections (numbers, dates, and names of drug) were

91 ssociation between cumulative number of anti-VEGF injections and change from baseline in VA at 12 mon

92 The mean numbers of anti-VEGF injections over 12 months were similar: 5.6 (standa

93 year and stratified based on number of anti-VEGF injections received over 1 year.

94 Self-reports of anti-VEGF injections were collected.

95 ease linearly with increasing number of anti-VEGF injections.

96 morphologic and functional outcomes of anti-VEGF therapy, the largest conducted to date in nAMD, ide

97 an eye size appears to be the driver of anti-VEGF treatment duration and therefore, dosing interval n

98 vating the RAAS reduced the efficacy of anti-VEGF.

99 and the effect of race and ethnicity on anti-VEGF efficacy to ensure optimal treatment for each indiv

100 In eyes with exudative AMD, previous anti-VEGF treatments did not impact retinal vascular measurem

101 sion, and the average duration of prior anti-VEGF therapy was approximately 2 years.

102 Eyes were included if they had received anti-VEGF injections for a period of at least 4 years and had

103 Consecutive patients with nAMD received anti-VEGF therapy according to a T&E (n = 163) or PRN (n = 10

104 Among these, 164 eyes received anti-VEGF therapy and 1003 eyes received laser therapy.

105 lated macular degeneration who received anti-VEGF treatment were included.

106 surgical planning in patients receiving anti-VEGF injections, especially in those with a primary tube

107 group of DME patients receiving regular anti-VEGF treatment without lapses.

108 re was the mean number of self-reported anti-VEGF injections.

109 of patients received chronic and serial anti-VEGF injections.

110 n = 474; Switzerland, n = 321) starting anti-VEGF for nAMD in routine clinical practice between Janua

111 At 2 years after starting anti-VEGF therapy, almost 1 in 10 eyes showed BCVA at the lev

112 r number of injections, suggesting that anti-VEGF injections may have a modest effect on the RNFL thi

113 s across the study groups revealed that anti-VEGF treated patients with wet AMD, who showed no exudat

114 omplications after tube revision in the anti-VEGF group included 5 explanted tubes for recurrent eros

115 To extend the anti-VEGF loading dose from 3 to 6 injections necessitates in

116 retina to inhibit angiogenic stimuli to anti-VEGF agents, which inhibit pathologic angiogenesis but a

117 clear whether these features respond to anti-VEGF therapies differently.

118 for nonadherence and nonpersistence to anti-VEGF therapy as well as studies examining strategies to

119 aocular cytokines and responsiveness to anti-VEGF therapy, which indicated a possible link to underly

120 re associated with anatomic response to anti-VEGF therapy.

121 phenotypes and potential responders to anti-VEGF therapy.

122 l trial environment but were related to anti-VEGF treatment administered in normal clinical practice.

123 AS improves patients' responsiveness to anti-VEGF.

124 ents showed a higher odds of treatment (anti-VEGF: OR = 1.35; 95%CI, 1.02-1.77; P < 0.001; bevacizuma

125 t lapse in patients with DME undergoing anti-VEGF therapy.

126 Of these, 63.6% (n = 6379) were anti-VEGF agents, and 36.4% (n = 3656) were PRP treatments.

127 st-Protocol S: -77; P = 0.005), whereas anti-VEGF rates increased from 876/1000 in 2012 to 1583/1000

128 erapy; however, it is not clear whether anti-VEGF treatment is causative of atrophy versus being asso

129 Protocol S, PRP rates decreased, while anti-VEGF rates increased.

130 umber of tube erosions in patients with anti-VEGF (15 tubes, 4.8%) versus without anti-VEGF (12 tubes

131 This figure covaried significantly with anti-VEGF agent according to the patient age at first injecti

132 -eight percent of patients treated with anti-VEGF agents experienced an SMH within 30 days of anti-VE

133 comes in patients with RVO treated with anti-VEGF agents.

134 However, limitations associated with anti-VEGF medications require to unravel new pathways of vess

135 ortheast patients who were treated with anti-VEGF showed a higher odds of receiving ranibizumab or af

136 n Asian patients, treatment of AMD with anti-VEGF therapy yielded 12-month visual outcomes comparable

137 showed visual and anatomic benefit with anti-VEGF therapy, most often observed shortly after initiati

138 curs in the context of MNV treated with anti-VEGF therapy; however, it is not clear whether anti-VEGF

139 In patients treated with anti-VEGF, 19 (45%) had a stable treatment interval, 5 (12%)

140 ti-VEGF (15 tubes, 4.8%) versus without anti-VEGF (12 tubes, 2.6%) (P = 0.10).

141 Patients with and without anti-VEGF injections were compared.

142 er treatment with brolucizumab or other anti-VEGFs.

143 order to predict patients' responses to anti-VEGFs and to identify key mechanisms that underpin the d

144 rein we determine first the response to anti-VEGFs, using spectral-domain optical coherence tomograph

145 IF or HIF-responsive growth factors, such as VEGF, for the treatment of cancers caused by VHL inactiv

146 These results indicate an autocrine VEGF neuroprotection on RGCs.

147 get genes in PAECs stimulated with TGF-beta, VEGF or serotonin.

148 by reproducing the known affinities between VEGF-A(165a):VEGFR1 and VEGF-A(165a):VEGFR2, 1.0 pM and

149 uring a brief window a few days after birth, VEGF inhibition induced rapid and profound remodeling of

150 cells infiltration, indicating that blocking VEGF-C signaling can reduce local chronic inflammation a

151 nib, a tyrosine kinase inhibitor that blocks VEGF receptors, into a non-inflammatory biodegradable po

152 Furthermore, both VEGF and NRP-1 knockdown inhibit the growth of patient-d

153 udy provides evidence convincingly that both VEGF and FGF mediate their biological action through a c

154 RUNX1 expression, which was downregulated by VEGF modulation.

155 f VE-cadherin (chip assay) and is induced by VEGF in DPSCs.

156 compared these effects with those induced by VEGF-A.

157 ory feedback loop, which can be modulated by VEGF.

158 isation and whether that can be prevented by VEGF blockade.

159 ery) and vascular permeability (triggered by VEGF-A).

160 X1 and vascular endothelial growth factor-C (VEGF-C) signaling.

161 GF-A), vascular endothelial growth factor-C (VEGF-C) were positive controls overexpressed into the HN

162 on for vascular endothelial growth factor-C (VEGF-C), that of maintaining the integrity of the BM per

163 tion of pro(lymph)angiogenic VEGF-A, VEGF-C, VEGF-D and infiltration of macrophages.

164 Vegfc in club cell secretory protein (CCSP)/VEGF-C mice reduced macrophage accumulation and fibrosis

165 However, their role in controlling VEGF A and FGF 2 signaling in the CL of water buffalo is

166 of TNF-alpha, IL-6, IL-12p70, IL-10, GM-CSF, VEGF, MIP-1beta, TNF-beta, IFN-alpha2 and IL-7 in respon

167 Increased concentrations of the cytokine VEGF-A in the cornea are associated with HSK severity.

168 18a was shown to increase TSP-1 and decrease VEGF by reducing PAI-1 (plasminogen activator inhibitor-

169 ression of oncogenes involved in PDGF, EGFR, VEGF, insulin/IGF/MAPKK, FGF, Hedgehog, TGFbeta, and PI3

170 baseline vascular endothelial growth factor (VEGF) (880.0 pg/mL vs 245.4 pg/mL; P = .012) and decreas

171 its both vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF) with the aim of

172 Vascular endothelial growth factor (VEGF) and semaphorin-binding receptor Neuropilin-1 (Nrp-

173 1alpha), vascular endothelial growth factor (VEGF) and tumor necrosis factor-alpha (TNF-alpha) may re

174 arin and vascular endothelial growth factor (VEGF) could be implanted into the arterial system of a p

175 in anti-vascular endothelial growth factor (VEGF) drug.

176 argeting vascular endothelial growth factor (VEGF) has transformed therapy for these proliferative re

177 approved vascular endothelial growth factor (VEGF) inhibitor, or a combination of both, were administ

178 VT) anti-vascular endothelial growth factor (VEGF) injections, which places a substantial burden on p

179 olarized vascular endothelial growth factor (VEGF) secretion, and matched iPSC-RPE monolayers to the

180 ncreased vascular endothelial growth factor (VEGF) stimulation due to a reduced capacity to re-synthe

181 sed anti-vascular endothelial growth factor (VEGF) therapy intensity and its relationship with visual

182 ved anti-vascular endothelial growth factor (VEGF) treatment for macular neovascularization (MNV).

183 Anti-vascular endothelial growth factor (VEGF) treatment of neovascular age-related macular degen

184 (PCNA), vascular endothelial growth factor (VEGF), and osteopontin (OPN) in the DPSC + THSG group we

185 etion of vascular endothelial growth factor (VEGF), brain-derived neurotrophic factor, fibroblast gro

186 (EGFR), Vascular endothelial growth factor (VEGF), etc.

187 ncluding vascular endothelial growth factor (VEGF), where it enhances local histone H3 acetylation an

188 bitor of vascular endothelial growth factor (VEGF)-C and VEGF-D.

189 ied that vascular endothelial growth factor (VEGF)-C, a potent lymphangiogenic factor, is up-regulate

190 restrain vascular endothelial growth factor (VEGF)-induced angiogenesis, spatially restrict expressio

191 hermore, vascular endothelial growth factor (VEGF)-induced EC migration was diminished in YY1-deplete

192 tions of vascular endothelial growth factor (VEGF)-neutralizing antibodies.

193 hepatic vascular endothelial growth factor (VEGF)-stromal cell-derived factor 1 (sdf1) signaling, le

194 ation of vascular endothelial growth factor (VEGF).

195 ME (anti-vascular endothelial growth factor [VEGF], focal laser treatment, steroids, or observation),

196 targets, including the proangiogenic factors VEGF and PDGF.

197 We measured the binding kinetics for VEGF-A(165), -A(165b), and -A(121) with VEGFR1 and VEGF-

198 were 0.10 fg/mL for DSG3, and 0.20 fg/mL for VEGF-A, VEGF-C and beta-Tub.

199 rentiating the splice variants in all future VEGF-A studies.

200 The combination inhibited orthotopic growth, VEGF-A expression, and tumor vasculature of both TNBC an

201 es and growth factors (CSF2, IL-6, TNF, HGF, VEGF, and EGF), ATM and p53 signaling pathways.

202 Active RhoC elevated HSP90alpha, HIF1alpha, VEGF expression, and angiogenesis in the human bladder c

203 ain endothelial cells (BECs) secreted higher VEGF (vascular endothelial growth factor) and lower TSP-

204 Here we report that immobilized VEGF captures blood circulating monocytes (MC) with high

205 versus 27 +/- 2 nm in controls, p < 0.05) in VEGF-treated hearts relative to controls.

206 non-OSA patients, whereas no differences in VEGF levels emerged.

207 Cs demonstrated 3.2-fold in HGF, 2.9-fold in VEGF and 8.7-fold in PDGF-B higher gene expressions comp

208 itol-(4,5)-bisphosphate (PIP2), resulting in VEGF-exacerbated defects in angiogenesis and angiogenic

209 algorithm with an alternative which includes VEGF testing for all patients with an acquired demyelina

210 sitive regulation on the HIF2alpha-increased VEGF-A expression that resulted in increasing VEGF-A in

211 EGF-A expression that resulted in increasing VEGF-A in the VHL-wt RCC cells.

212 , via suppression of COUP-TFII level, induce VEGF-C overexpression.

213 oned supernatant of DMOG-treated HSC induced VEGF-dependent proliferation of LSEC.

214 Interestingly, VEGF promoted norrin signaling by increasing the FZD4 co

215 ator, especially the earliest-known isoform, VEGF-A(165a).

216 the age of 3 years, trigger factors, and low VEGF serum levels.

217 Introducing mandatory VEGF testing for patients with acquired demyelinating ne

218 , we and others showed that P130CAS mediates VEGF-A and PDGF signalling in vitro, but its cardiovascu

219 hod was implemented to generate monodisperse VEGF encapsulated microcarriers.

220 Most VEGF-induced changes in gene expression were not reverse

221 Multiple VEGF inhibitors are now approved for the treatment of cc

222 Neutralizing VEGF-A in vivo using bevacizumab inhibited sympathetic i

223 at the tubulogenic effect of GW0742, but not VEGF-A, was PPARbeta/delta- and sirtuin-1-dependent.

224 Exogenous administration of VEGF-C via an adenoassociated viral vector improved hema

225 These results reveal the capacity of VEGF-C to promote immune surveillance of tumours, and su

226 Baseline concentrations of VEGF and MCP-1 are associated with anatomic response to

227 The duration of VEGF exposure influenced both barrier relaxation and ant

228 in rodent BPD models, severe side effects of VEGF therapy prevent its use in patients with BPD.Object

229 y, eMSCs upregulated intrinsic expression of VEGF and CNTF and their receptors.

230 Relative mRNA expression of VEGF in the cornea was quantified by using qPCR.

231 then result in increasing the expression of VEGF-A and VEGF-C via targeting the 3'UTR of mRNAs at a

232 We found a significant increase of VEGF-A, VEGF-C, and Ang1 levels in U-HAE patients compar

233 As such, bevacizumab-based inhibition of VEGF has been the clinically adopted strategy to treat c

234 Pharmacological inhibition of VEGF signaling phenocopied the pax2a(-/-) vasculature, F

235 Conversely, inhibition of VEGF signaling prevents excessive angiogenic sprouting o

236 Intravitreal OPT-302 inhibition of VEGF-C and -D was well tolerated, and OPT-302 combinatio

237 oma has been revolutionised by inhibitors of VEGF receptor.

238 myeloid cells produced pathogenic levels of VEGF-A within HSV-1-infected corneas, and CD4(+) cell de

239 thelial cells, where ADMA in the presence of VEGF-induced endothelial cell signaling for F-actin stre

240 stand the role of EGR mediated regulation of VEGF A and FGF 2 signaling in buffalo luteal cells.

241 The differential regulation of VEGF-A vs VEGF-C by AR may then result in differential i

242 d a neurotrophic and neuroprotective role of VEGF, albeit in retina, cellular mechanisms underlying t

243 tient-derived GBM cells expressing shRNAs of VEGF or neuropilin-1 (NRP-1) attenuate cancer stem cell

244 Previous studies of VEGF-A:VEGFR binding have measured binding kinetics for

245 forkhead box F1), both downstream targets of VEGF, can improve lung structure and function after neon

246 olonged survival in mice compared to that of VEGF depletion.

247 The upregulation of VEGF and IL-18 was detected in PDR.

248 -C expression, yet this miR-185-5p effect on VEGF-A was reversed via AR's positive regulation on the

249 Only VEGF-A stimulated HUVEC migration and proliferation wher

250 tion is suggested by its ability to overcome VEGF antagonism.

251 In parallel, VEGF produced by mixed retinal cells or by mesenchymal s

252 PDGF/VEGF ligands regulate a plethora of biological processes

253 e the first evidence in a metazoan of a PDGF/VEGF ligand acting as a myokine that regulates systemic

254 However, the mechanisms of PROX1/VEGF-C feedback loop remain poorly understood.

255 seline to 12 and 24 months in eyes receiving VEGF inhibitors, whereas clinically significant IOP elev

256 tly reduced microvessel density and secreted VEGF levels.

257 e cells (GCs) or by prolonged brain-specific VEGF overexpression culminating in extensive, highly sel

258 up received FND cauterization and subsequent VEGF TrapR(1)R(2) eye drops three times per day whereas

259 d increase miR-185-5p expression to suppress VEGF-C expression, yet this miR-185-5p effect on VEGF-A

260 endothelial ENG was attenuated by targeting VEGF signaling with an anti-VEGFR2 (VEGF receptor 2) ant

261 he vicious cycle of inflammation, COUP-TFII, VEGF-C, and lymphangiogenesis in the endometriotic micro

262 y in human breast cancer, demonstrating that VEGF-C strongly correlates with activation of Hedgehog s

263 (RGCs) in culture, we demonstrated here that VEGF is released by RGCs themselves to promote their own

264 Therefore, we tested the hypothesis that VEGF-induced vascular leak can acutely increase atrial a

265 It was observed that VEGF A and FGF 2 induced angiogenesis, cell proliferatio

266 Pursuit of such candidates revealed that VEGF used multiple, nonredundant effectors to relax the

267 We show that VEGF-C, secreted by breast cancer cells that have underg

268 Taken together, these data suggest that VEGF can acutely predispose otherwise normal hearts to a

269 Here, we report for the first time that VEGF-C signaling is necessary for valve morphogenesis.

270 t AEs were consistent with inhibition of the VEGF and HGF pathways.

271 nsistent with the plausible reduction of the VEGF autocrine stimulation of RGCs.

272 PROX1 promotes the expression of the VEGF-C receptor VEGFR3 in lymphatic endothelial cells (L

273 Our study suggests that the VEGF-C/NRP2/GLI axis is a novel and conserved paracrine

274 n retina, cellular mechanisms underlying the VEGF neuroprotection remain elusive.

275 factor 1alpha (HIF1alpha) to upregulate the VEGF.

276 Thus, VEGF-A can shape the sensory and sympathetic nerve lands

277 ssels with a mode-of-action complementary to VEGF-R (vascular endothelial growth factor receptor)-tar

278 er in cells that were chronically exposed to VEGF (hours instead of minutes).

279 er in cells that were chronically exposed to VEGF.

280 therapy may overcome an escape mechanism to VEGF-A suppression in the management of nAMD.

281 X1 expression in LVs and LVVs in response to VEGF-C signaling.

282 Evaluation of EV-transmitted VEGF-C from patients' sera demonstrates it is a reliable

283 In turn, VEGF-C signaling maintains PROX1 expression in LECs.

284 eries offer a new paradigm for understanding VEGF-A, while further stressing the need to take care in

285 monstrated that the anti-angiogenic variant, VEGF-A(165b) selectively prefers VEGFR2 binding at an af

286 models representing different steps in VEGFA/VEGF receptor 2 (VEGFR2)-induced vascular permeability,

287 argeting VEGF signaling with an anti-VEGFR2 (VEGF receptor 2) antibody.

288 noradrenaline to stimulate angiogenesis via VEGF signaling and enhance the rate of tumor growth.

289 In vitro, VEGF-A from infected corneas repressed sensory nerve gro

290 The differential regulation of VEGF-A vs VEGF-C by AR may then result in differential impacts on

291 Our goal was to identify effectors by which VEGF and anti-VEGF control the endothelial cell barrier

292 mselves to promote their own survival, while VEGF neutralization by specific antibodies or traps dras

293 an microvascular EC, with an additivity with VEGF.

294 Combining FND cauterization with VEGF TrapR(1)R(2) treatment prevented the undesired effe

295 Finally, glaucomatous patients injected with VEGF traps (ranibizumab or aflibercept) due to either AM

296 ymphatic vasculature can be manipulated with VEGF-C to promote an immune response to glioblastoma.

297 were increased with norrin and VEGF or with VEGF alone, but both norrin and VEGF were required for e

298 luate DCN localization and relationship with VEGF pathway via in situ hybridization maps and RNA sequ

299 cells were then cultured and stimulated with VEGF A and FGF 2.

300 y in eyes receiving long-term treatment with VEGF inhibitors as previously feared.