ライフサイエンスコーパス: VEGF-A

1 VEGF-A and EGFR expression was determined by immunohisto

2 VEGF-A and ID1 expression was examined in peritoneal bio

3 VEGF-A and nitric oxide are essential for glomerular fil

4 VEGF-A and p-Ser166-Mdm2 protein levels were measured in

5 VEGF-A antibody was added into the preservation solution

6 VEGF-A blockade in alpha-VEGF D/-, alpha-VEGF D/R, and a

7 VEGF-A blockade in tumors was associated with HIF1alpha

8 VEGF-A blockade was investigated in an orthotopic rat mo

9 VEGF-A directly contributes to the formation of a reperf

10 VEGF-A is a promising target for molecular fluorescence

11 VEGF-A isoforms showed differential ERK1/2 and p38 MAPK

12 VEGF-A pre-mRNA is alternatively spliced at the terminal

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

14 VEGF-A regulation through ID1 was confirmed by siRNA in

15 VEGF-A stimulated proliferation of MM cells in monolayer

16 VEGF-A stimulates signal transduction pathways that modu

17 VEGF-A was immunolocalized to peritoneal mesothelium and

18 VEGF-A was increased in peritoneal fluid from women with

19 VEGF-A was measured in peritoneal fluid by ELISA (n = 16

20 VEGF-A, an angiogenic factor, is increased in the perito

21 VEGF-A-dependent Mdm2 phosphorylation was demonstrated i

22 as a central mediator of STAT3, HIF-1alpha, VEGF-A and angiogenesis via multiple signalling mechanis

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

24 sult of the increased expression of VEGFR-2, VEGF-A, VEGF-C, and VEGF-D.

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

26 rmined tumor uptake of (89)Zr-bevacizumab, a VEGF-A-binding PET tracer, in mRCC patients before and d

27 was only improved with the adjuvant use of a VEGF-A/Ang2-bispecific CovX-body (CVX-241) but not when

28 lidate vascular endothelial growth factor A (VEGF-A) and epidermal growth factor receptor (EGFR)-targ

29 ted by vascular endothelial growth factor A (VEGF-A) by way of a VEGF receptor-2 (VEGFR-2) primed act

30 lowing vascular endothelial growth factor A (VEGF-A) exposure.

31 mented vascular endothelial growth factor A (VEGF-A) expression and induction of arteriogenesis.

32 2) and vascular endothelial growth factor A (VEGF-A) expression.

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

34 human vascular endothelial growth factor A (VEGF-A) gene, a known EGR1-responsive gene, revealed mod

35 ), and vascular endothelial growth factor A (VEGF-A) genes.

36 reased vascular endothelial growth factor A (VEGF-A) has been implicated in the pathogenesis of choro

37 by the vascular endothelial growth factor A (VEGF-A) in endothelial tip cells of the mouse retina.

38 Vascular endothelial growth factor A (VEGF-A) is a master regulator of angiogenesis, vascular

39 Vascular endothelial growth factor A (VEGF-A) is a potent proangiogenic cytokine elevated in p

40 factor vascular endothelial growth factor A (VEGF-A) is subject to a multitude of stimulus-dependent,

41 Tumor vascular endothelial growth factor A (VEGF-A) level may be useful.

42 Vascular endothelial growth factor A (VEGF-A) produced locally is supposed to play an importan

43 reduce vascular endothelial growth factor A (VEGF-A) production by tumor cells.

44 Vascular endothelial growth factor A (VEGF-A) regulates many aspects of vascular physiology.

45 of all vascular endothelial growth factor A (VEGF-A) splice isoforms from the kidney results in prote

46 ion in vascular endothelial growth factor A (VEGF-A) stimulated HREC cultures.

47 x, and vascular endothelial growth factor A (VEGF-A) was carried out at selected time points.

48 els of vascular endothelial growth factor A (VEGF-A), a key regulator of angiogenesis.

49 bulin, Vascular Endothelial Growth Factor A (VEGF-A), and clusterin compared to the control group.

50 nesis, vascular endothelial growth factor A (VEGF-A), and platelet-derived growth factor B chain (PDG

51 erived vascular endothelial growth factor A (VEGF-A), interleukin 10 (IL-10) and prostaglandin E2 (PG

52 ctors [vascular endothelial growth factor A (VEGF-A), platelet-derived growth factors (PDGFs), and no

53 lly by vascular endothelial growth factor A (VEGF-A).

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

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

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

57 actors vascular endothelial growth factor-A (VEGF-A) and angiopoietin-1 are constitutively expressed

58 Vascular endothelial growth factor-A (VEGF-A) is thought to be a critical mediator of vascular

59 erived vascular endothelial growth factor-A (VEGF-A) promotes tumor progression and angiogenesis.

60 human vascular endothelial growth factor-A (VEGF-A) results in the expansion and directed differenti

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

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

63 Vascular endothelial growth factor-A (VEGF-A), the best known angiogenic factor, was originall

64 orm of vascular endothelial growth factor-A (VEGF-A), VEGF-A165b, in human obesity.

65 cts of vascular endothelial growth factor-A (VEGF-A/VEGF) and its receptors on endothelial cells func

66 ascular endothelial growth factor isoform A (VEGF-A) and islet vascularization on beta-cell function

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

68 An adenovirus expressing VEGF-A (Ad-VEGF-A(164)) replicates the tumor vasculature in mice wi

69 c vessel type to form in tumors and after Ad-VEGF-A(164).

70 As in tumors, Ad-VEGF-A(164) strikingly increased endothelial nitric oxid

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

72 change in the NOD2-responsive NO, TNF-alpha, VEGF-A, and IL-12 levels was observed.

73 p was found among GCF endocan and TNF-alpha, VEGF-A, CAL, and GI for all groups (P <0.05).

74 Although VEGF-A failed to support an enduring vascular response,

75 In contrast, although VEGF-A is required for maintaining the specialized vascu

76 Here we analyzed VEGF-A isoform-specific stimulation of VCAM-1 gene expre

77 HIF1A and VEGF A (VEGFA) mRNA, a transcriptional target of HIF-1,

78 The VEGF-C/VEGFR-3 and VEGF-A/VEGF-R2 signaling pathways are two of the best-st

79 s and binds to the AP-1 site at the IL-6 and VEGF-A promoters.

80 RC cells contained higher levels of IL-6 and VEGF-A than that from vector control cells and significa

81 lls via osteoblast-derived interleukin-6 and VEGF-A, thereby upregulating MMP-9.

82 Fos to enhance the transcription of IL-6 and VEGF-A, which promotes angiogenesis in CRC.

83 ionally activated the expression of IL-6 and VEGF-A.

84 Ang2 and VEGF-A treatment rescued angiogenesis in Nox2-silenced c

85 nib also inhibited chronic PDGF-A and -B and VEGF-A and -B expressions.

86 d state in the presence of both TGF-beta and VEGF-A.

87 if treated simultaneously with TGF-beta and VEGF-A.

88 GF-beta signaling molecules, Tenascin-C, and VEGF-A, while pro-fibrotic molecules, including several

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

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

91 Both endocan and VEGF-A levels were higher in plasma of patients with inv

92 le microvasculature to insulin, exercise and VEGF-A and reduce microvascular density.

93 onnect between HIF-1alpha protein levels and VEGF-A expression.

94 ith SLE; we found that lymphangiogenesis and VEGF-A were increased in the lymph nodes of mice with co

95 fect on the bone marrow microenvironment and VEGF-A/VEGFR targeting restores bone marrow function.

96 ased BMP signaling and increased osterix and VEGF-A.

97 nd pool 7 induced phospho-SMAD, osterix, and VEGF-A, which is indicative of increased bone morphogene

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

99 ced superoxide formation and Ang2, Tie2, and VEGF-A expression.

100 In HPMEC, LPS-induced Ang2, Tie2, and VEGF-A protein expression was preceded by increased supe

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

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

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

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

105 -A knockout and overexpression of angiogenic VEGF-A isoforms each worsen diabetic nephropathy.

106 Concentrations of angiogenic (VEGF-A, Ang1, Ang2), anti-angiogenic (VEGF-A165b ) and l

107 Anti-VEGF-A therapies also have immunologic effects that may

108 received intravenous bevacizumab-800CW (anti-VEGF-A), cetuximab-800CW (anti-EGFR), control tracer IgG

109 ed with elevated levels of an antiangiogenic VEGF-A splice isoform (VEGF-A165b) and a corresponding r

110 tion-driven expression of the antiangiogenic VEGF-A isoform can contribute to impaired collateralizat

111 provide new insights into mechanisms behind VEGF-A-regulated transcriptional programs in endothelial

112 t cancer showed inverse correlations between VEGF-A expression and CD8(+) T cell infiltration, and a

113 Mice lacking NRP1 or NRP1-binding VEGF-A isoforms have defective RGC axon organisation alo

114 t (sFlt), an angiogenic inhibitor that binds VEGF-A, significantly decreased the amount of blood vess

115 ATF-2 knockdown blocked VEGF-A-stimulated VCAM-1 expression and endothelial-leuk

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

117 reduced filopodia extension, which are both VEGF-A-dependent processes.

118 y by preventing Cdc42 and Pak2 activation by VEGF-A and Slit2.

119 in tumor growth and angiogenesis induced by VEGF-A in vitro and in vivo.

120 Tumor growth and angiogenesis induced by VEGF-A, histamine, and serotonin are almost completely i

121 d moderately in endothelial cells induced by VEGF-A.

122 This proliferation is inhibited by VEGF-A/VEGFR-2 blockade.

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

124 that TR3-TVs are differentially regulated by VEGF-A and identify a novel signaling pathway by which V

125 ized monoclonal antibody against circulating VEGF-A, when added to CCNU chemotherapy in patients with

126 sion-driven HuR translocation and consequent VEGF-A mRNA stabilization were absent in Myh9(-/-) macro

127 preclinical models, the angiogenic cytokine VEGF-A has been identified as a critical regulator of NM

128 E-1, soluble VEGFR1, VEGF-A, VEGF-C, VEGF-D, VEGF-A isoform 121, bone morphogenetic protein 7, macrop

129 defects are caused exclusively by defective VEGF-A signalling in RGCs or are exacerbated by abnormal

130 red, both epidermal and myeloid cell-derived VEGF-A contributed to regeneration-induced tumorigenesis

131 ons of epidermal versus myeloid cell-derived VEGF-A during HPV-mediated tumorigenesis, with possible

132 ion of epidermal versus myeloid cell-derived VEGF-A in HPV-mediated skin cancer by interbreeding an H

133 Although only epidermal-derived VEGF-A was essential for initiation of skin tumor develo

134 Tumor-derived VEGF-A, PLGF-2, and VEGF-B augment pain sensitivity thro

135 mediated miR-150 transfer and miR-150-driven VEGF-A/VEGFR/PI3K/Akt pathway activation, thereby modula

136 Serum and GCF endocan, VEGF-A, and TNF-alpha levels were significantly higher i

137 To establish VEGF-A isoform expression and functional effects in IPF.

138 An adenovirus expressing VEGF-A (Ad-VEGF-A(164)) replicates the tumor vasculature

139 alpha protein levels, and to a lesser extent VEGF-A levels, in renal cystadenoma cells in a Tsc2+/- m

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

141 reduced expression of the angiogenic factor VEGF-A.

142 lated expression of the proangiogenic factor VEGF-A and by increased tumor angiogenesis.

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

144 ombinant vascular endothelial growth factor (VEGF-A) and tumor-induced VEC-Y658 phosphorylation in vi

145 downstream of the angiogenic growth factors VEGF-A and Slit2.

146 For VEGF-A, highly polarized receptor distribution contribut

147 in GSNOR(-/-) MSCs, a receptor essential for VEGF-A action in MSCs.

148 RK, p38, and JNK) pathways are important for VEGF-A-induced TR3-TV2 and TR3-TV3 mRNA induction.

149 ovascular capillaries to be the location for VEGF-A-induced leakage, as expressed by significantly hi

150 showed ATF-2 to be functionally required for VEGF-A-stimulated endothelial VCAM-1 gene expression.

151 s have previously revealed a requirement for VEGF-A, the class 3 semaphorin SEMA3C, and their shared

152 ransmembrane receptors and was distinct from VEGF-A-induced neuronal growth.

153 , these data indicate that excess glomerular VEGF-A and eNOS deficiency is necessary and sufficient t

154 Importantly, the MAOA-dependent HIF1alpha/VEGF-A/FOXO1/TWIST1 pathway was activated in high-grade

155 -enhanced miR-185-5p also promotes HIF2alpha/VEGF-A expression via binding to the promoter region of

156 Immunohistochemistry showed high VEGF-A expression in 79%-96% and high EGFR expression in

157 at TP53 mutations are associated with higher VEGF-A expression (P = 0.006).

158 A recent paper describes how VEGF-A stimulates paracrine secretion of hepatocyte grow

159 in response to acute exercise and identified VEGF-A as a key stimulator of Mdm2 phosphorylation on Se

160 red human cells and that immunoprecipitating VEGF-A results in protein that is detected by VEGF-A165b

161 a transcription factor highly implicated in VEGF-A and VEGF-C gene regulation.

162 of TGF-beta1 and ID1 has been implicated in VEGF-A regulation during tumor angiogenesis.

163 forms of AMD, suggesting that an increase in VEGF-A has a direct age-dependent adverse effect on RPE

164 In vivo, IC generation resulted in VEGF-A-dependent intranodal lymphangiogenesis and increa

165 sion of HIF2alpha-dependent genes, including VEGF-A, PAI-1, and cyclin D1 in ccRCC cell lines and tum

166 Clinical trials including VEGF-A administration for therapeutic angiogenesis have

167 In KRIT1-depleted cells, increased VEGF-A levels led to increased VEGF receptor 2 (VEGFR2)

168 Exercise increased VEGF-A and p-Ser166-Mdm2 protein levels respectively by

169 The data support a central role of increased VEGF-A not only in the pathogenesis of neovascular but a

170 Mice with overall increased VEGF-A levels develop progressive morphological features

171 These findings suggest that increased VEGF-A leads to an age-dependent RPE and retinal dysfunc

172 and retinal thinning in mice with increased VEGF-A levels correlate with progressive age-dependent a

173 +/-)LoxP-VEGF-A(+/+) to conditionally induce VEGF-A isoform deletion specifically in the alveolar typ

174 er FcgammaR cross-linking by IC might induce VEGF-A and lymph node lymphangiogenesis.

175 Similarly, IC-induced VEGF-A production by B cells was inhibited by FcgammaRII

176 on of the features of CSCs with EMT-induced, VEGF-A-mediated angiogenesis as the connecting mechanism

177 Instead, VEGF-A acts via the neuropilin-1 (NRP-1) co-receptor.

178 ted and funneled by PRKD2 into the NF-kappaB/VEGF-A signaling axis to promote tumor angiogenesis and

179 displayed reduced expression of KLF2, KLF4, VEGF-A, VEGF-C, and FGFR3 and elevated expression of p57

180 s on tumor uptake of the radioactive-labeled VEGF-A antibody bevacizumab with PET in NET patients.

181 mice, with decreased angiopoietin-1 levels, VEGF-A upregulation, decreased soluble VEGF receptor-1 (

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

183 zumab (an antibody to the angiogenic ligand, VEGF-A) in breast cancer have found improved responses i

184 ansgenic mouse SPC-rtTA(+/-)TetoCre(+/-)LoxP-VEGF-A(+/+) to conditionally induce VEGF-A isoform delet

185 Macrophage VEGF-A production, ischemic tissue VEGF-A levels, and fl

186 genotype showed increased FcgammaR-mediated VEGF-A production, demonstrating a similar process is li

187 These results suggest that c-Kit-mediated VEGF-A action in beta-cells plays a pivotal role in main

188 expression, suggesting that mTORC1 mediates VEGF-A expression via both HIF-1alpha-dependent and -ind

189 IIA in signal transduction events modulating VEGF-A expression in tissue.

190 VEGFR) 2 as well as VEGF signaling molecules VEGF-A, VEGF-C, and VEGF-D.

191 tes from HD mice and patients contained more VEGF-A, which triggers proliferation of endothelial cell

192 r defects through modulation of the Akt/mTOR/VEGF-A pathway, indicating that c-Kit signaling in beta-

193 Multiple VEGF-A isoforms exist, but the biological significance o

194 splicing leads to the generation of multiple VEGF-A isoforms, including VEGF165.

195 Aflibercept ('VEGF Trap', which neutralizes VEGF-A, VEGF-B and PlGF) showed greater efficacy than ne

196 S6K1 inhibition reduces HIF-1alpha but not VEGF-A expression, suggesting that mTORC1 mediates VEGF-

197 hat mutant GlyRS-mediated disruption of Nrp1/VEGF-A signalling is permissive to maturation and mainte

198 in contrast to the proangiogenic activity of VEGF-A.

199 ted culture system reinforced by addition of VEGF-A, VEGF-C, and EGF most efficiently generated LECs,

200 However, reduced extracellular binding of VEGF-A to Nrp1 is known to disrupt post-natal blood vess

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

202 Concentration of VEGF-A was further increased in patients with lower C1-I

203 Plasma concentrations of VEGF-A, VEGF-C, Ang1, and Ang2 were higher in patients w

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

205 monary fibrosis, ATII-specific deficiency of VEGF-A or constitutive overexpression of VEGF-A165b inhi

206 mice harboring myofiber-specific deletion of VEGF-A (mVEGF(-/-)) and in vitro in primary human and ro

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

208 mouse model with a conditional disruption of VEGF-A restricted to either epidermal or myeloid cells.

209 study, we sought to identify the effects of VEGF-A neutralization on parameters of glucose metabolis

210 determined whether peritoneal expression of VEGF-A is regulated by TGF-beta1 through the ID1 pathway

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

212 The expression of VEGF-A, VEGF-B, PlGF, VEGFR1, and VEGFR2 was measured in

213 A key feature of VEGF-A isoform-specific ERK1/2 activation and nuclear tr

214 We demonstrate that half of VEGF-A-regulated gene promoters are characterized by a t

215 The direct impact of VEGF-A on Treg induction was assessed together with spec

216 and serotonin receptors, are independent of VEGF-A, and are directly dependent on TR3/Nur77.

217 are phenocopied by intraocular injection of VEGF-A or pericyte-specific inactivation of the murine g

218 Effects of intravitreal injections of VEGF-A, VEGF-E, PlGF-1, and VEGF trap were also studied.

219 Conversely, introduction of VEGF-A specifically into BAT of obese mice restored vasc

220 VEGF antagonist that blocks all isoforms of VEGF-A in patients with neovascular age-related macular

221 intenance of this phenotype, as knockdown of VEGF-A gene expression or treatment with VEGF-A-inactiva

222 EGF-A165 and subsequently enhanced levels of VEGF-A signaling.

223 ere characterized by higher plasma levels of VEGF-A, VEGF-C, and Ang2 compared with the other patient

224 present study indicate that manipulation of VEGF-A splice isoforms could be a novel therapeutic aven

225 Surprisingly, the classical mechanism of VEGF-A action via interaction with VEGF receptors does n

226 vestigated the transcriptional regulation of VEGF-A-responsive genes in primary human aortic endothel

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

228 ily may be involved, but the precise role of VEGF-A, VEGF-B, placental growth factor (PlGF), and thei

229 s activation of HuR and its stabilization of VEGF-A mRNA were Rac2-dependent, and proteomic analysis

230 GF release (120 minutes) and upregulation of VEGF-A mRNA levels (24 hours).

231 fector of TGFbeta1 dependent upregulation of VEGF-A, and highlights a novel potential therapeutic tar

232 ssion of an antiangiogenic splice variant of VEGF-A.

233 osure to exendin-4, but not that of PDX-1 or VEGF-A/C.

234 All groups showed similar values for plasma VEGF-A and central foveal thickness measurements.

235 SUV(max) was not related to plasma VEGF-A at all scan moments.

236 Secondary outcomes were plasma VEGF-A and central foveal thickness.

237 ized uptake values were compared with plasma VEGF-A and time to disease progression.

238 e, we examined the effect of excess podocyte VEGF-A on the renal phenotype of endothelial nitric oxid

239 tic cells (DCs) stimulated with ICs produced VEGF-A, and this was inhibited by coligation of FcgammaR

240 S and p110alpha interaction prevented proper VEGF-A and FGF-2 signaling, which are required for effic

241 rAAV.VEGF-A, though stimulating angiogenesis, induced neither

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

243 We quantified the kinetics of the recent VEGF-A:PDGFRbeta interaction for the first time with KD

244 ineered single-chain version of pan-receptor VEGF-A with an N-terminal cysteine-containing tag for si

245 Recombinant VEGF-A elevated p-Ser166-Mdm2 by 50-125% and stimulated

246 and the 2 KLF proteins cooperate to regulate VEGF-A, VEGF-C, FGFR3, and p57 by binding to the regulat

247 In vitro FRS2alpha regulates VEGF-A and VEGF-C-dependent activation of extracellular

248 -1 cells and primary islets, c-Kit regulates VEGF-A expression via the Akt/mammalian target of rapamy

249 lear beta-catenin signaling and up-regulates VEGF-A protein expression.

250 Renal VEGF-A mRNA expression increased significantly with NaHS

251 to partially restore HIF1alpha and secreted VEGF-A levels in hypoxic cancer cells treated with HSP90

252 dings to autoimmunity because elevated serum VEGF-A has been observed in patients with SLE; we found

253 ts as a result of their expression of single VEGF-A isoforms.

254 promoting in vivo HIF-1alpha stabilization, VEGF-A production, and revascularization in the ischemic

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

256 Therapeutic intervention by targeting VEGF-A, VEGFR2, and VEGFR3 inhibited tumor growth, consi

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

258 More important, we found that VEGF-A or VEGF-E, but not VEGF-B, nor placenta growth fa

259 Here we report that VEGF-A and IGF-1 differ in their ability to stabilize ne

260 Here, we show that VEGF-A secretion, but not gene transcription, in either

261 We show that VEGF-A, histamine, IGFBP3, and LPA trigger unequal endot

262 These studies suggest that VEGF-A acts via interaction with NRP-1 to trigger intrac

263 The VEGF-A isoforms play a crucial role in vascular developm

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

265 xamined the vasculoprotective effects of the VEGF-A isoform VEGF-A165b in diabetic nephropathy.

266 Within only 72 h of administration of the VEGF-A-neutralizing monoclonal antibody B.20-4.1, we obs

267 therapies, specifically those targeting the VEGF-A/VEGFR2 pathway, have been approved for subsets of

268 ntravitreal aflibercept injections and their VEGF-A concentrations assayed by multiplex bead analysis

269 , but the overall beneficial effects of this VEGF-A targeting agent are relatively modest, in part du

270 Thus, ICs contribute to inflammation through VEGF-A-driven lymph node lymphangiogenesis, which is con

271 acrophage VEGF-A production, ischemic tissue VEGF-A levels, and flow recovery to hind limb ischemia w

272 EGF -/R resulted in neutralization of tissue VEGF-A.

273 fferent functional behavior when compared to VEGF-A or TGF-beta treatment alone.

274 longs to the VEGF family, but in contrast to VEGF-A, VEGF-B does not regulate blood vessel growth.

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

276 lations that were intrinsically resistant to VEGF-A blockade did not exhibit any of these features, c

277 elanomas that are intrinsically resistant to VEGF-A blockade do not show any evidence of compensatory

278 Tumor xenografts that initially responded to VEGF-A inhibition underwent an adaptation in vivo, leadi

279 study, we examined the adaptive response to VEGF-A inhibition by a loss-of-function analysis using p

280 s, melanomas that are initially sensitive to VEGF-A blockade acquire adaptive resistance by adopting

281 and 4E-BP1 regulate HIF-1alpha translation, VEGF-A is primarily under the control of 4E-BP1/eIF4E.

282 tendency to be coordinately transcribed upon VEGF-A stimulation.

283 rowth factor, soluble TIE-1, soluble VEGFR1, VEGF-A, VEGF-C, VEGF-D, VEGF-A isoform 121, bone morphog

284 revascularization and relapse, in part, via VEGF-A release.

285 osts promote VEC proliferation, probably via VEGF-A signaling, whereas IFNgamma shows an antiangiogen

286 by macrophages within the bridge, which via VEGF-A secretion induce a polarized vasculature that rel

287 eatment is associated with decreased vitreal VEGF-A levels in wet AMD patients.

288 1) had significantly lower levels of vitreal VEGF-A (141.11 +/- 61.89 pg/mL) when compared with group

289 Primary outcome was vitreal VEGF-A levels (at the time of anti-VEGF injection).

290 sub-podocyte space coverage is reduced when VEGF-A is depleted, all of which are rescued in VEGF-A16

291 and growth of SC endothelial cells, whereas VEGF-A obliterated the aqueous outflow system.

292 identify a novel signaling pathway by which VEGF-A and VEGF-E, but neither VEGF-B, nor PlGF, induce

293 but extend the molecular mechanism, by which VEGF-A-induced angiogenesis.

294 ic disease-particularly, in combination with VEGF-A blockers (but not VEGFR2 TKIs) in resected breast

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

296 current findings linking TP53 mutation with VEGF-A upregulation offered a mechanistic explanation fo

297 ly higher rate of fluorophore spreading with VEGF-A injection when compared to vehicle control (26+/-

298 In addition, treatment with VEGF-A decreased S-nitrosylated laminin in cultured podo

299 of VEGF-A gene expression or treatment with VEGF-A-inactivating antibody reduces these responses.

300 lar dysfunction in diabetic nephropathy, yet VEGF-A knockout and overexpression of angiogenic VEGF-A