ライフサイエンスコーパス: VEGF

1 VEGF antagonism also increased markers of endothelial ce

2 VEGF binding to its cognate receptor, VEGFR2, activates

3 VEGF is also a chondrocyte survival factor during develo

4 VEGF-A protein expression was determined by enzyme-linke

5 VEGF-A stimulated proliferation of MM cells in monolayer

6 VEGF-A165 b rescues the increase in glomerular basement

7 VEGF-A165 b restores the expression of platelet endothel

8 a variety of growth factors, such as IGF-1, VEGF-alpha, TGF-beta, and Wnt proteins that regulate epi

9 These data demonstrate that the HIF-1alpha/VEGF-A axis is an essential aspect of tumor immunity.

10 th factor (VEGF)-A, -C, and VEGF receptor 2 (VEGF-R2) in VECs was assessed by real-time PCR.

11 (34) VEGF enhances ETS1 chromatin occupancy and increases ETS

12 on mRCC patients with (89)Zr-bevacizumab, a VEGF-A-binding antibody tracer.

13 Q8 elicits antiangiogenic effects in a VEGF-independent in vitro model of angiogenesis and exer

14 the pancreatic cancer vasculature through a VEGF-independent mechanism.

15 and alters tumor vessel parameters through a VEGF-independent mechanism.Angiogenesis is essential for

16 hibits vascular endothelial growth factor A (VEGF-A) expression.

17 ion of vascular endothelial growth factor A (VEGF-A).

18 9) and vascular endothelial growth factor A (VEGF-A).

19 gands, vascular endothelial growth factor-A (VEGF-A), contributing to neurodegeneration.

20 BDNF), vascular endothelial growth factor-A (VEGF-A), insulin-like growth factor-1 (IGF-1) and Klotho

21 e isoforms of vascular endothelial growth A (VEGF) each have different affinities for the extracellul

22 coding vascular endothelial growth factor-A [VEGF-A] or thymosin beta 4 [Tbeta4]) was applied regiona

23 vascular endothelial growth factor (VEGF)-A, VEGF-C, FGFR3, and p57/CDKN1C genes.

24 f EVs, called microvesicles (MVs), activates VEGF receptors and tumour angiogenesis through a unique

25 Surprisingly, 100% of adult ADN-VEGF-C mice developed chylothorax within 7 days.

26 he findings indicate that chylothorax in ADN-VEGF-C mice results from retrograde flow of chyle from t

27 adult mice, the LVs showed regression after VEGF-C or VEGFR3 deletion, administration of the tyrosin

28 Bevacizumab, a monoclonal antibody against VEGF, improves the proportion of patients responding to

29 were immunostained using an antibody against VEGF.

30 umab, a monoclonal antibody directed against VEGF, improves outcomes when added to platinum-based che

31 the context of progressive depletion of all VEGF-A isoforms from the podocytes.

32 Flow cytometry was used to analyze VEGF-R2 expression in corneal CD31 cells, and VEGF-A and

33 ule-1, vascular cell adhesion protein-1, and VEGF.

34 route through the regulation of miR-185 and VEGF isoforms.

35 associated with a decrease of HIF-1alpha and VEGF expression within tumors.

36 n of iNOS and arginase, as well as MMP-9 and VEGF.

37 ly expressed and responded to VEGF-A165a and VEGF-A165b in terms of proliferation and matrix expressi

38 functional isoforms including VEGF-A165a and VEGF-A165b, a member of the inhibitory family.

39 serum (TNF-alpha, IL-6, IL-12, TGF-beta, and VEGF) were down regulated by DMDD.

40 s reduce light-induced secretion of bFGF and VEGF to near normal levels.

41 endothelial growth factor (VEGF)-A, -C, and VEGF receptor 2 (VEGF-R2) in VECs was assessed by real-t

42 -thirds were downregulated including CA9 and VEGF-A.

43 EGF-R2 expression in corneal CD31 cells, and VEGF-A and IFNgamma expression in corneal CD4 T cells.

44 decreased growth, blood vessel density, and VEGF and hypoxia-inducible factor 1alpha (HIF-1alpha) ex

45 -directed biopsies revealed enriched MIF and VEGF at the enhancing edge in bevacizumab-naive patients

46 ma transcriptionally activates PDGFRbeta and VEGF.

47 EC coculture increased VEC proliferation and VEGF-A protein expression, whereas blocking VEGF-A signi

48 ch have well-defined roles in Semaphorin and VEGF signaling, positively regulate HH pathway function,

49 fined coreceptor for class 3 semaphorins and VEGF, plays important roles in the immune system; howeve

50 C mesothelial-to-mesenchymal transition, and VEGF-A production.

51 so reduced the number of CD31(+) vessels and VEGF-A-positive cells in fibrotic peritoneum.

52 L25, IL-2RB, IL-15RA, CD6) and angiogenesis (VEGF-A) were significantly increased only in AD.

53 Outside the breeding season (BS), angiogenic VEGF-A stimulates vessel growth in the infundibulum, aid

54 Anti-VEGF injection frequency per treated eye over a 1-year p

55 Anti-VEGF treatment is often experienced with some anxiety re

56 There were 959 945 anti-VEGF injections among 124 835 patients from 2006 to 2015

57 own whether these effects differ across anti-VEGF agents.

58 further show that prototype long-acting anti-VEGF drugs (LAVAs) that include this peptide attenuate V

59 The reduced vascular density after anti-VEGF treatment further decreased delivery in these tumor

60 ese tumors, the impaired response after anti-VEGF treatment is directly linked to strong deposition o

61 7.1% to 10.2% and 17.2% to 26.4% among anti-VEGF groups for NPDR and PDR eyes, respectively.

62 bevacizumab is important in choosing an anti-VEGF drug for the hundreds of thousands of patients with

63 educe the risk of CNVM development, and anti-VEGF therapy for CNVM was associated with better clinica

64 op combined therapies using anti-AR and anti-VEGF-C compounds to better suppress ccRCC progression.Th

65 Intra-articular anti-VEGF antibodies suppress OA progression, reduce levels o

66 d in combination with bevacizumab (BEV, anti-VEGF), it could reverse the adverse effects that precipi

67 payments to ophthalmologists, biologic anti-VEGF agents ranibizumab and aflibercept accounted for 95

68 ents from 2013 to 2014 were analyzed by anti-VEGF agent, payment category, and dollar amount.

69 observational study that commenced anti-VEGF treatment for nAMD between January 2006 and January

70 ful cataract surgery treated with early anti-VEGF treatment.

71 leted the study had lower than expected anti-VEGF injection rates.

72 nti-vascular endothelial growth factor (anti-VEGF) drugs can cause phenotypic alteration and maturati

73 nti-vascular endothelial growth factor (anti-VEGF) injections from 2012 to 2013.

74 r endothelial growth factor inhibitors (anti-VEGF) for wet age-related macular degeneration (wAMD), a

75 (i.e., no treatment); (2) intravitreal anti-VEGF injection; (3) verteporfin photodynamic therapy (vP

76 Intravitreal anti-VEGF injections are widely used in the treatment of wet-

77 otal and annual numbers of intravitreal anti-VEGF injections, as well as injections per 1000 enrolled

78 00 mg daily (n = 3), with intravitreous anti-VEGF therapy using predefined retreatment criteria.

79 Monthly anti-VEGF injections were given until a dry macula was achiev

80 e at month 6 after monthly injection of anti-VEGF agents for treating ME due to CRVO and HRVO.

81 The mean number of anti-VEGF injections for an eye with mCNV during the first ye

82 ms barriers surrounding the delivery of anti-VEGF injections to patients with mCNV.

83 retinal thickness, fluid; and number of anti-VEGF injections.

84 bfield retinal thickness, and number of anti-VEGF injections.

85 treatment (134/135; 99.3%) consisted of anti-VEGF injections; 0.7% (1/135) received vPDT.

86 th no difference found between types of anti-VEGF medications (P = 0.896).

87 Intravitreal injections of anti-VEGF medications increased annually from 2006 to 2015.

88 ged over the past 40 years; the role of anti-VEGF therapy remains to be established in current treatm

89 The potential role of anti-VEGF treatment for type 1 ROP has become a focus in rece

90 rimary outcomes included the effects of anti-VEGF treatment on development of peripheral retinal vess

91 frequent in patients at early stages of anti-VEGF treatment.

92 r GL261 gliomas received POL5551 and/or anti-VEGF antibody B20-4.1.1.

93 Those who received anti-VEGF payments were more likely to use ranibizumab or afl

94 She received anti-VEGF therapy to prevent further vision loss and retinal

95 likely to resolve in eyes that received anti-VEGF treatment prior to study participation (OR, 0.33; 9

96 ee hundred patients with wAMD receiving anti-VEGF treatment and 100 patient carers were recruited.

97 1 and 2 years, eyes with NPDR receiving anti-VEGF treatment for DME may experience improvement in DR

98 Patients and mice receiving anti-VEGF/VEGFR drugs develop hypertension, reflecting system

99 within hours, a single dose of several anti-VEGF drugs collapsed MV to form glomeruloid microvascula

100 In the United States, anti-VEGF injection was the most frequently utilized treatmen

101 events, events associated with systemic anti-VEGF therapy, and events not associated with systemic an

102 and events not associated with systemic anti-VEGF therapy.

103 This supports the idea that anti-VEGF agents are effective in reducing the amount of VEGF

104 leukemia on in vivo VEGF capture by the anti-VEGF antibody bevacizumab.

105 ditive antiangiogenic response with the anti-VEGF biologic bevacizumab.

106 ination therapy group compared with the anti-VEGF monotherapy group.

107 roviders (74%), greater than 90% of the anti-VEGF payments were associated exclusively with either ra

108 there are distinct ocular advantages to anti-VEGF pharmacotherapy for some cases (such as eyes with z

109 tumors in which adaptive resistance to anti-VEGF therapy (B20 antibody) developed.

110 rained model to predict the response to anti-VEGF therapy for tumors expressing different levels of V

111 iposomes, restored tumor sensitivity to anti-VEGF therapy.

112 1, 1.50); p=0.54] for events related to anti-VEGF treatment, and 1.11 [ (0.87, 1.40); p=0.40] for eve

113 r predicting how tumors will respond to anti-VEGF treatment, and it complements pre-clinical in vivo

114 could successfully predict response to anti-VEGF treatment, the reduction in tumor volume.

115 .40); p=0.40] for events not related to anti-VEGF treatment.

116 Together, anti-VEGF/VEGFR drugs act in part by inhibiting eNOS, causing

117 erious adverse events between these two anti-VEGF drugs; i.e., relative risks of >/=1.5 are unlikely.

118 angle of resolution [logMAR] 0.00 with anti-VEGF and 0.20 without; P = 0.018).

119 ticosteroids, but subjects treated with anti-VEGF had better visual outcomes (12-month median visual

120 Those treated with anti-VEGF injections showed significant improvement in VA at

121 e eyes and eyes treated previously with anti-VEGF, which will allow study results to have broad appli

122 in the BS, melatonin releases antiangiogenic VEGF-Axxxb from the PT, inhibiting infundibular angiogen

123 m before treatment (MIG, IL22, TRAIL, APRIL, VEGF, IL3, TWEAK, SCF, IL21), identified patients who de

124 ability are driven by growth factors such as VEGF and pro-inflammatory cytokines such as TNF-alpha.

125 (LAVAs) that include this peptide attenuate VEGF-induced retinal changes in animal models of neovasc

126 molecular interrogation reveals an atypical VEGF-based vasculogenesis signalling that facilitates re

127 king M2 macrophage-derived factors TGF-beta, VEGF and SDF-1 abolished VEGFR1(+) myeloid cell migratio

128 py should be much more effective in blocking VEGF signaling to EKR1/2.

129 VEGF-A protein expression, whereas blocking VEGF-A significantly reduced VEC proliferation (P = 0.04

130 e communication and retention are boosted by VEGF thereby impairing adipogenesis.

131 These deposits were increased by VEGF antagonism, a common wet ARMD treatment, suggesting

132 Angiogenic responses induced by VEGF had no effect in either HSP70-1 siRNA in vitro or H

133 n of glycine transporter 1(GlyT1) induced by VEGF led to an increase in intracellular glycine.

134 ely on specialized vasculature maintained by VEGF that is produced by neighboring epithelial cells, t

135 in sub-podocyte space coverage, produced by VEGF-A depletion.

136 Endothelial-enriched PCs (CD34(+)/VEGF(+)) were independent predictors of mortality in pat

137 SRC-2 knockdown in cardiomyocytes decreased VEGF expression and secretion to levels sufficient to bl

138 b to be ineffective in blocking MV-dependent VEGF receptor activation.

139 Dysregulation of RPE- and podocyte-derived VEGF is associated with neovascularization in wet age-re

140 We detected VEGF expression in JG cells of control mice, and cAMP ag

141 in II and hypoxia, respectively, which drive VEGF expression.

142 mulates expression of Kdr, the gene encoding VEGF receptor 2, in murine embryonic gonads.

143 Endogenous VEGF signalling prevents excess neovessel pericyte cover

144 uction, suggesting that the use of exogenous VEGF expression as a therapeutic for neovascularization

145 ation of Akt by the potent angiogenic factor VEGF-A does not strongly stabilize microtubules or suffi

146 levels of the lymphangiogenic growth factor VEGF-D are elevated significantly in lymphangioleiomyoma

147 = .01); vascular endothelial growth factor (VEGF) (Group I: 157.0 (154.0) pg/mL, Group II: 98.0 (20.

148 the anti-vascular endothelial growth factor (VEGF) agent ranibizumab (Lucentis; Roche, Basel, Switzer

149 of anti-vascular endothelial growth factor (VEGF) agents.

150 romoting vascular endothelial growth factor (VEGF) and matrix metalloproteinase (MMP) 13.

151 against vascular endothelial growth factor (VEGF) and platelet-derived growth factor.

152 VD), and vascular endothelial growth factor (VEGF) expression) from 9 patients with primary ccRCC.

153 ncreased vascular endothelial growth factor (VEGF) expression.

154 Vascular endothelial growth factor (VEGF) is implicated in the peritoneal membrane remodelin

155 TIONALE: Vascular endothelial growth factor (VEGF) is the main driver of angiogenesis and vascular pe

156 Vascular endothelial growth factor (VEGF) level was highly co-stained in endothelial cells b

157 ation of vascular endothelial growth factor (VEGF) or endonuclease III-like protein 1 (NTHL1) genes.

158 requires vascular endothelial growth factor (VEGF) originating from outside the blood-brain barrier,

159 ogic and vascular endothelial growth factor (VEGF) pathways have failed to demonstrate tumor control.

160 lator of vascular endothelial growth factor (VEGF) receptor activation.

161 show how vascular endothelial growth factor (VEGF) regulates PRKCB promoter function in CLL cells, st

162 iency of vascular endothelial growth factor (VEGF) results in thrombotic microangiopathy, we addresse

163 tance of Vascular Endothelial Growth Factor (VEGF) secretion for this pathway of hypoxia-mediated sel

164 ms along vascular endothelial growth factor (VEGF) signaling pathways at concentrations too low to be

165 wed that vascular endothelial growth factor (VEGF) signaling within the glomeruli of Alport mice is s

166 Anti-vascular endothelial growth factor (VEGF) therapy has demonstrated efficacy in treating huma

167 ith anti-vascular endothelial growth factor (VEGF) therapy may provide information useful in counseli

168 pts anti-vascular endothelial growth factor (VEGF) therapy-induced glioma growth and dissemination.

169 ing anti-vascular endothelial growth factor (VEGF) therapy.

170 ing anti-vascular endothelial growth factor (VEGF) treatment.

171 1alpha), vascular endothelial growth factor (VEGF), hypoxia-inducible factor 1-alpha (HIF-1alpha) and

172 promoter vascular endothelial growth factor (VEGF), is therefore an attractive strategy for inhibitin

173 against vascular endothelial growth factor (VEGF), is used clinically to treat certain types of meta

174 6, IL-8, vascular endothelial growth factor (VEGF), monocyte chemoattractive protein 1 (MCP-1), and g

175 utralize vascular endothelial growth factor (VEGF), such as aflibercept or ranibizumab, rescue vision

176 ncluding vascular endothelial growth factor (VEGF), that normally stimulate multiple phases of wound

177 ction of vascular endothelial growth factor (VEGF), while matrices displaying pathological levels of

178 Vascular endothelial growth factor (VEGF)-A has been implicated in this context, but there a

179 xon-8 of vascular endothelial growth factor (VEGF)-A results in production of proangiogenic VEGFxxxa

180 ssion of vascular endothelial growth factor (VEGF)-A, -C, and VEGF receptor 2 (VEGF-R2) in VECs was a

181 ting the vascular endothelial growth factor (VEGF)-A, VEGF-C, FGFR3, and p57/CDKN1C genes.

182 vWF) and vascular endothelial growth factor (VEGF)-C expression were measured.

183 ssion of vascular endothelial growth factor (VEGF)-C was driven by the adipocyte-specific promoter ad

184 Vascular endothelial growth factor (VEGF)-D is capable of inducing angiogenesis and lymphang

185 ium in a vascular endothelial growth factor (VEGF)-independent manner.

186 example, vascular endothelial growth factor (VEGF)-mediated angiogenesis is inhibited upon reduction

187 duced by vascular endothelial growth factor (VEGF).

188 ofile of vascular endothelial growth factor (VEGF)165/VEGF165b transcripts was relevant to SRSF6 expr

189 ted with vascular endothelial growth factor (VEGF-A) and tumor necrosis factor (TNF)-alpha levels.

190 ecules (VCAM-1), endothelial growth factors (VEGF) and VDBP.

191 ed in both human and murine tumors following VEGF signaling blockade, resulting in recruitment of CX3

192 ic growth factor distribution distinctly for VEGF and PlGF, and to buffer free VEGF and PlGF levels i

193 xide/ssDNA (GO-ssDNA) on an Au-electrode for VEGF detection, and incorporated with poly-L-lactide nan

194 de liner detection ranges (0.05-100ng/mL for VEGF and 1-100ng/mL for PSA), as well as high levels of

195 l correlate, and support a critical role for VEGF-D in lung vascular development and homeostasis.

196 inctly for VEGF and PlGF, and to buffer free VEGF and PlGF levels in tissue.

197 Furthermore, VEGF/ERK signaling induces phosphorylation and activatio

198 yofiber VEGF is required for the hippocampal VEGF response to acute exercise.

199 nces in signaling by soluble and immobilized VEGF, to a multi-scale whole-body framework.

200 that Gsalpha knockout may result in impaired VEGF production.

201 e next examined a potential role of PTP1B in VEGF-induced angiogenesis.

202 duces multiple functional isoforms including VEGF-A165a and VEGF-A165b, a member of the inhibitory fa

203 elopment of MMD and TGF-beta in Treg induced VEGF.

204 ajor determinant of angiogenesis and induces VEGF transcription.

205 Moreover, calpain activation inhibited VEGF-induced VEGFR2 phosphorylation, which can be restor

206 Overexpression of PTP1B inhibited VEGF-induced VEGFR2 and Akt phosphorylation in bovine ao

207 atively regulates angiogenesis by inhibiting VEGF expression.

208 ious studies suggest that the splice isoform VEGF-A165 b (resulting from alternative usage of a 3' sp

209 sprouting angiogenesis) is required for its VEGF-mediated induction.

210 uate correlation between GCF endocan levels, VEGF-A, and TNF-alpha levels with periodontal probing de

211 itration of NO-Tie2 signalling and localized VEGF induction, suggesting that the use of exogenous VEG

212 and tumor growth by modulating Sp1-mediated VEGF expression.

213 covered a novel role of calpain in mediating VEGF-induced PI3K/AMPK/Akt/eNOS activation through Ezrin

214 ch based on VEGF-immobilized microparticles (VEGF-MPs).

215 is study demonstrates that skeletal myofiber VEGF is required for the hippocampal VEGF response to ac

216 ents are effective in reducing the amount of VEGF present in the retina.

217 icate that changes in the bioavailability of VEGF-A sourced from ATII cells, namely the ratio of VEGF

218 r, little is known about the contribution of VEGF-A splice isoforms to kidney physiology and patholog

219 Deletion of VEGF-A, an HIF target gene, in CD8(+) T cells accelerate

220 The discovery of VEGF-PDGFRs binding challenges this paradigm and calls f

221 The model predicts the existence of VEGF threshold in ERK1/2 activation that can be continuo

222 eatment inhibited intratumoral expression of VEGF and tumor vascularization.

223 melatonin-induced differential expression of VEGF-A isoforms culminates in alterations in gonadotroph

224 ad-transgenic model, that over-expression of VEGF-A165 b alone is sufficient to rescue the increase i

225 kinase inhibitor sunitinib, or expression of VEGF-C/D trap, which also compromised the lymphatic drai

226 angiogenesis through a unique 90 kDa form of VEGF (VEGF90K).

227 portant embryonic and postnatal functions of VEGF can be reconciled with an apparently destructive ro

228 The importance of VEGF produced by ALL cells in mediating leukemia-cell en

229 er heightened when therapeutic inhibition of VEGF receptor 2 (VEGFR2) is utilized in combination with

230 Inhibition of VEGF signalling increases pericyte coverage in microvess

231 ed angiogenesis was blocked by inhibition of VEGF with sFlt1 (from 881 +/- 98% increase in functional

232 Tivozanib, a pan-inhibitor of VEGF receptors, reduced proliferation of the chemoresist

233 py for tumors expressing different levels of VEGF receptors.

234 ssion slightly increased the basal levels of VEGF, but did not block the inhibitory effect of RAD001

235 Furthermore, levels of VEGF-D and MCP-1 in patient sera correlated positively w

236 y identifies YAP/TAZ as central mediators of VEGF signaling and therefore as important regulators of

237 ild on our previous systems biology model of VEGF transport and kinetics in tumor-bearing mice to inc

238 reased both MSC homing and MSC production of VEGF and IL-10, suggesting microenvironmental changes fr

239 sourced from ATII cells, namely the ratio of VEGF-Axxxa to VEGF-Axxxb, are critical in development of

240 The regulation of VEGF by IPMK requires its catalytic activity.

241 gate the role of VEGFR3 in the regulation of VEGF-induced vascular permeability.

242 The release of VEGF could be sustained for 4weeks.

243 there is no clear information on the role of VEGF-A in IPF.

244 n vivo require ETS1-mediated transduction of VEGF signaling to release paused RNAPII.

245 This also acts on VEGF receptor 2 (VEGFR2) expressed in PD prolactin-produ

246 , we report a pro-survival approach based on VEGF-immobilized microparticles (VEGF-MPs).

247 L-6 receptor (sIL-6R) alone had no effect on VEGF production, stimulation of HPMCs with IL-6 in combi

248 not block the inhibitory effect of RAD001 on VEGF.

249 ng durable responses in pazopanib- and other VEGF inhibitor-refractory tumors, which supports epigene

250 d pathways, and decreases the level of PGK1, VEGF and HIF-1alpha in vitro and in vivo.

251 ion of these peptides by lentivirus prevents VEGF-induced capillary network formation in Matrigel plu

252 ith IL-6 in combination with sIL-6R promoted VEGF expression and secretion through a transcriptional

253 high expression of tight junction proteins, VEGF-dependent permeability, efflux pump activity and re

254 As a result, rAAV.Tbeta4 but not rAAV.VEGF-A improved EF in db hearts (34.5 +/- 1.4%), but les

255 ngs could be relevant for patients receiving VEGF antagonists.

256 inding of Sp1 to the VEGF promoter to reduce VEGF expression.

257 phenotypic effect was accompanied by reduced VEGF expression and angiogenesis, diminished numbers of

258 of control mice, and cAMP agonists regulated VEGF expression in cultured renin-producing cells.

259 have been largely attributed to up-regulated VEGF expression.

260 be detected in serum within 1 day, and serum VEGF levels are suppressed for at least 8 to 12 weeks.

261 es in model systems expressing only a single VEGF isoform.

262 the promoter of miR-185-5p, which suppresses VEGF-C expression via binding to its 3' UTR.

263 UB cells synthesize VEGF-A and PDGF-BB proteins and RNA, whereas the MM cell

264 -cell entry into the CNS, which by targeting VEGF signaling may serve as a novel strategy to control

265 ease in expression of the HIF-1alpha targets VEGF-A, glucose transporter-1, and lactate dehydrogenase

266 increases endothelial permeability and that VEGF has no additive effect, suggesting a common pathway

267 In this study, we demonstrated that VEGF-dependent activation of the Src/FAK/paxillin signal

268 Addressing these questions, we find that VEGF acts as a survival factor in growth plate chondrocy

269 s of both ARMD and TMA, we hypothesized that VEGF and CFH interact.

270 how similar protection, thus indicating that VEGF trapping is a potentially viable mechanism for AFSC

271 Mechanistically, we show that VEGF activates YAP/TAZ via its effects on actin cytoskel

272 These data suggest that VEGF expressed by skeletal myofibers may directly or ind

273 Together, these results suggest that VEGF protects the retinal and glomerular microvasculatur

274 a common wet ARMD treatment, suggesting that VEGF inhibition could reduce cellular complement regulat

275 The VEGF(f/f) trained group showed improvements in both spee

276 The VEGF(HSA-/-) group did not.

277 s injection of an AAV2 vector expressing the VEGF-neutralising protein sFLT01 in patients with advanc

278 Differential splicing of the VEGF-A gene produces multiple functional isoforms includ

279 f valine to methionine at residue 118 of the VEGF-D protein.

280 ich then inhibited the binding of Sp1 to the VEGF promoter to reduce VEGF expression.

281 Mechanistically, LKB1 could bind to the VEGF transcription factor, specificity protein 1 (Sp1),

282 or enrichment of HIF-1alpha protein and thus VEGF.

283 hage-derived cytokine, eotaxin, IL10, TIMP1, VEGF, TGFbeta1, and TGFbeta2, along with changes in tiss

284 TII cells, namely the ratio of VEGF-Axxxa to VEGF-Axxxb, are critical in development of pulmonary fib

285 retinal vascular endothelial cells (ECs) to VEGF-A, leading to upregulation of angiopoietin-2 (Ang2)

286 PTP1B), and the relevance of this pathway to VEGF-induced angiogenesis, especially in diabetic wound

287 ts differentially expressed and responded to VEGF-A165a and VEGF-A165b in terms of proliferation and

288 erbated vascular permeability in response to VEGF, administered via intradermal adenoviral delivery o

289 A showed faster wound closure in response to VEGF.

290 GF(f/f) , untrained VEGF(HSA-/-) and trained VEGF(HSA-/-) mice, but not trained VEGF(f/f) mice.

291 d trained VEGF(HSA-/-) mice, but not trained VEGF(f/f) mice.

292 P < 0.05) in untrained VEGF(f/f) , untrained VEGF(HSA-/-) and trained VEGF(HSA-/-) mice, but not trai

293 llenge decreased CBF (P < 0.05) in untrained VEGF(f/f) , untrained VEGF(HSA-/-) and trained VEGF(HSA-

294 f angiogenesis and vascular permeability via VEGF receptor 2 (VEGFR2), whereas lymphangiogenesis sign

295 and lymphangiogenesis through signaling via VEGF receptor (VEGFR)-2 and VEGFR-3, respectively.

296 pecific reduction of CNS leukemia on in vivo VEGF capture by the anti-VEGF antibody bevacizumab.

297 nds on the "angiogenic signal" produced when VEGF binds to its receptors on tumor endothelial cells.

298 Here, we investigated whether VEGF release by HPMCs is controlled by IL-6 in combinati

299 esults define an angiogenic pathway in which VEGF enhances ETS1-BRD4 interaction to broadly promote R

300 conditions, but also highly correlated with VEGF-A and Klotho.

301 cts of DA with a focus on its relations with VEGF and hypoxia inducible factor related angiogenesis p

302 of retinal endothelial cells stimulated with VEGF.