ライフサイエンスコーパス: VPF

1 VPF caused normal venules to leak ferritin, and, as pred

2 VPF-Class is a tool that automates the taxonomic classif

3 VPF/VEGF acts selectively on the vascular endothelium to

4 VPF/VEGF and its receptors may play an important but as

5 VPF/VEGF induced dermal microvascular EC expression of m

6 VPF/VEGF induces vascular hyperpermeability, cell divisi

7 VPF/VEGF mRNA and protein were, however, strongly expres

8 VPF/VEGF mRNA was also expressed focally at lower levels

9 VPF/VEGF stimulates endothelial cell growth and increase

10 ctor/vascular endothelial growth factor-164 (VPF/VEGF(164)) into the ears of athymic mice.

11 tif, dephosphorylates Ser(290) Mutating (257)VPF(259) eliminated PP1 binding and blunted dephosphoryl

12 ays an important role in preventing aberrant VPF/VEGF overexpression and the angiogenesis that result

13 scites tumor, which itself secretes abundant VPF/VEGF.

14 ant negative mutant RhoA-19N does not affect VPF/VEGF-stimulated KDR phosphorylation, intracellular C

15 by visceral glomerular epithelial cells, and VPF/VEGF may be an important regulator of glomerular end

16 VPF/VEGF induction of EC gene expression and VPF/VEGF enhancement of microvascular permeability, sugg

17 rotein phosphorylation and localization, and VPF-induced permeability.

18 avbeta3 heterodimer at the cell surface, and VPF/VEGF also induced mRNA encoding osteopontin (OPN), a

19 OPN promoted EC migration in vitro; and VPF/VEGF induction of alphavbeta3 was accompanied by inc

20 otent beta-CN-derived peptides, VPV, YPI and VPF having DPP-IV IC(50) values of 6.6 +/- 0.5, 35.0 +/-

21 s with a plasmid overexpressing PKC zeta and VPF/VEGF promoter luciferase constructs results in activ

22 in 9L-conditioned medium was removed by anti-VPF antibodies, we examined dexamethasone effects of VPF

23 Applying VPF-Class on 731K uncultivated virus contigs from the IM

24 Subsequently, as VPF/VEGF(164) expression declined, glomeruloid bodies de

25 In addition, because VPF/ VEGF is also an endothelial growth factor, the loss

26 nt of OPN's adhesive properties, and because VPF/VEGF promotes increased microvascular permeability l

27 also illustrate an operational link between VPF/VEGF induction of EC gene expression and VPF/VEGF en

28 Thymosin beta-10 expression was modulated by VPF/VEGF and was strikingly down-regulated in senescent

29 GF (V-) cells expressed reduced constitutive VPF/VEGF and no detectable mouse VPF/VEGF, and formed sm

30 imulating angiogenesis and that constitutive VPF/VEGF expression dramatically promotes tumor coloniza

31 In the RefSeq database, VPF-class reported an accuracy of nearly 100% to classif

32 -1 pancreatic carcinoma cells, Sp1-dependent VPF/VEGF transcription is controlled by IGF-1R signaling

33 The Sp1-dependent VPF/VEGF transcription is regulated mainly by IRS-2.

34 cells PKC-zeta leads to direct Sp1-dependent VPF/VEGF transcription; in addition, it also promotes a

35 VPFs from the IMG/VR database and developed VPF-Class.

36 In many glomerular diseases, VPF/VEGF-expressing cells were decreased in number or ab

37 Tumor cells expressed VPF/VEGF mRNA strongly in only one case of KS, adjacent

38 Locally expressed VPF/VEGF(164) induced an early increase in microvascular

39 infected local cells that strongly expressed VPF/VEGF(164) mRNA for 10 to 14 days, after which expres

40 ls, immediately adjacent to cells expressing VPF/VEGF(164).

41 tor/vascular endothelial cell growth factor (VPF/VEGF) can both potently enhance vascular permeabilit

42 y factor/vascular endothelial growth factor (VPF/VEGF) exerts its multiple functions by activating tw

43 y factor/vascular endothelial growth factor (VPF/VEGF) functions by activating two receptor tyrosine

44 y factor/vascular endothelial growth factor (VPF/VEGF) functions by activating two receptor-tyrosine

45 y factor/vascular endothelial growth factor (VPF/VEGF) has been shown to be up-regulated in the vicin

46 y factor/vascular endothelial growth factor (VPF/VEGF) is a multifunctional cytokine and growth facto

47 y factor/vascular endothelial growth factor (VPF/VEGF) is considered to be the most important directl

48 y factor/vascular endothelial growth factor (VPF/VEGF) likely regulates endothelial cells (EC) migrat

49 y factor/vascular endothelial growth factor (VPF/VEGF) promotes its function primarily by activating

50 y factor/vascular endothelial growth factor (VPF/VEGF), a multifunctional cytokine, is regulated by d

51 y factor/vascular endothelial growth factor (VPF/VEGF), a potent angiogenic factor, by interacting di

52 y factor/vascular endothelial growth factor (VPF/VEGF), a potent cytokine expressed by most malignant

53 y factor/vascular endothelial growth factor (VPF/VEGF), significantly delays senescence in human derm

54 y factor/vascular endothelial growth factor (VPF/VEGF), the critical molecule in tumor angiogenesis,

55 y factor/vascular endothelial growth factor (VPF/VEGF).

56 y factor/vascular endothelial growth factor (VPF/VEGF, VEGF-A) is a multifunctional cytokine with imp

57 factor (VEGF)/vascular permeability factor (VPF) (phVEGF165) was delivered locally using a hydrogel-

58 factor (VEGF)/ vascular permeability factor (VPF) is an endothelial cell (EC) mitogen.

59 ed as a potent vascular permeability factor (VPF) that importantly contributes to vascular pathobiolo

60 Vascular permeability factor (VPF), also known as vascular endothelial growth factor (

61 Vascular permeability factor (VPF), also known as vascular endothelial growth factor (

62 factor (VEGF)/vascular permeability factor (VPF), an endothelial cell (EC)-specific mitogen, stimula

63 also known as vascular permeability factor (VPF), has been shown to increase potently the permeabili

64 also known as vascular permeability factor (VPF), is a key mediator of angiogenesis for both physiol

65 ed as a potent vascular permeability factor (VPF), suggesting that other vascular permeabilizing agen

66 dentified as a vascular permeability factor (VPF).

67 eted cytokine, vascular permeability factor (VPF).

68 t described as vascular permeability factor (VPF).

69 Vascular permeability factor (VPF)/vascular endothelial growth factor (VEGF) achieves

70 Vascular permeability factor (VPF)/vascular endothelial growth factor (VEGF) is an ang

71 member of the vascular permeability factor (VPF)/VEGF family of proteins, is an important angiogenic

72 rier function; vascular permeability factor (VPF, also known as vascular endothelial growth factor, V

73 wth factor (VEGF)/vascular permeable factor (VPF) expression, regulates leukocyte infiltration throug

74 zing the vaccinia virus processivity factor (VPF).

75 The signaling cascade that follows VPF/VEGF interaction with cultured endothelium is only p

76 d MAPK phosphorylation are not essential for VPF/VEGF-induced HUVEC migration.

77 sidues 1059 and 951 of KDR are essential for VPF/VEGF-induced HUVEC proliferation and migration, resp

78 has recently been shown to be important for VPF/VEGF mRNA stabilization.

79 data demonstrate cooperative mechanisms for VPF/VEGF regulation of EC migration involving the alphav

80 y, is a downstream event of IRS proteins for VPF/VEGF expression in AsPC-1 cells.

81 nd Gbetagamma subunits are also required for VPF/VEGF-stimulated HUVEC migration.

82 te that Gq/11 proteins are also required for VPF/VEGF-stimulated HUVEC proliferation.

83 ave shown that KDR is solely responsible for VPF/VEGF-induced human umbilical vein endothelial cell (

84 that KDR, but not Flt-1, was responsible for VPF/VEGF-induced human umbilical vein endothelial cell (

85 KDR is responsible for VPF/VEGF-stimulated endothelial cell (EC) proliferation

86 t has been shown that KDR is responsible for VPF/VEGF-stimulated endothelial cell (EC) proliferation

87 KDR is responsible for VPF/VEGF-stimulated endothelial cell proliferation and m

88 The action of dopamine was specific for VPF/VEGF and did not affect other mediators of microvasc

89 o performed immunohistochemical staining for VPF/VEGF protein in 15 cases.

90 ch the tumor cells stained substantially for VPF/VEGF protein.

91 To test this hypothesis, VPF was injected intradermally in normal animals after i

92 Of particular importance, VPF/VEGF was able to rescue senescent HDMEC, restoring t

93 scular peptides that regulate this important VPF function are currently unknown.

94 Flt-1-mediated antiproliferative activity in VPF/VEGF-stimulated endothelium.

95 Hippel Lindau (VHL) leads to an increase in VPF/VEGF expression.

96 1, p16 and p27) was significantly reduced in VPF/VEGF-treated cells but p53 expression was not signif

97 se C-zeta (PKC-zeta) plays a central role in VPF/VEGF expression and acts as a switching element.

98 unction and hence plays an important role in VPF/VEGF mediated angiogenesis.

99 We also observed that, in VPF/VEGF-stimulated HUVECs, the Flt-1/EGLT-mediated down

100 umor-derived permeability factors (including VPF), and reduction of VPF expression by tumor cells.

101 Thus, increased VPF/VEGF mRNA stability induced by hypoxia is mediated,

102 Here we report that hypoxia-induced VPF/VEGF expression is mediated by increased transcripti

103 ic tumor areas, and hypoxia potently induces VPF/VEGF expression in several tumor cell lines in vitro

104 g minimal constitutive and hypoxia-inducible VPF/VEGF.

105 ems to be an important stimulus for inducing VPF/VEGF mRNA expression in human mammary tumors.

106 al role of p53, through which it can inhibit VPF/VEGF expression by regulating the transcriptional ac

107 Atrial natriuretic peptide (ANP) inhibited VPF signaling, TJ protein phosphorylation and localizati

108 betagamma minigene, hbetaARK1(495), inhibits VPF/VEGF-stimulated HUVEC proliferation, MAPK phosphoryl

109 ntisense oligonucleotide completely inhibits VPF/VEGF-stimulated KDR phosphorylation.

110 At intervals after injecting VPF/VEGF i.p., mesenteries were harvested, extracted, an

111 In normal human kidney, VPF/VEGF mRNA and protein are strongly expressed by visc

112 at overexpress ANP showed significantly less VPF-induced kinase activation and vascular permeability

113 Like VPF, histamine and serotonin also stimulated ferritin ex

114 date the signaling mechanism of Ras-mediated VPF/VEGF transcriptional activation through PKCzeta and

115 t up to 4-fold in activation of Sp1-mediated VPF/VEGF transcription.

116 Both of the IRS proteins modulate VPF/VEGF expression in pancreatic cancer cells by differ

117 2 cells stably with sense or antisense mouse VPF/VEGF cDNA or with vector alone.

118 onstitutive VPF/VEGF and no detectable mouse VPF/VEGF, and formed small, minimally vascularized tumor

119 xpressed and secreted large amounts of mouse VPF/VEGF and formed well-vascularized tumors with hyperp

120 Neither VPF/VEGF mRNA or protein were strongly expressed in capi

121 ere relatively impermeable in the absence of VPF stimulation.

122 nase for PKC, the Ras-mediated activation of VPF/VEGF promoter through PKCzeta was further increased,

123 phatidylinositol 3-kinase, the activation of VPF/VEGF promoter through Ras, PDK-1, and PKCzeta was co

124 permeabilizing and angiogenic activities of VPF/VEGF.

125 mRNA level and also the promoter activity of VPF/VEGF.

126 al for releasing relatively large amounts of VPF/VEGF locally, leading to increased glomerular permea

127 bodies, we examined dexamethasone effects of VPF expression in 9L cells.

128 ety of glomerular diseases for expression of VPF/VEGF mRNA and protein by in situ hybridization and i

129 a by in situ hybridization for expression of VPF/VEGF, KDR, and flt-1 mRNAs.

130 tor by inhibiting the signaling functions of VPF that we define here and by preserving the endothelia

131 The implementation of VPF-Class can be downloaded from

132 Despite the importance of VPF information for viral discovery, VPFs have not yet b

133 hibited FCS- and PDGF-dependent induction of VPF expression.

134 ll established that the hypoxic induction of VPF/VEGF is in large part an increase in the stability o

135 by dexamethasone might involve inhibition of VPF action or expression, and if dexamethasone effects i

136 istent with this hypothesis, co-injection of VPF/VEGF together with OPN resulted in rapid cleavage of

137 ped a system that would allow measurement of VPF/VEGF-induced signaling on intact microvessels.

138 Decreased numbers of VPF/VEGF-expressing cells in glomeruli were also noted i

139 The Ras-mediated overexpression of VPF/VEGF was also found to be inhibited by using the ant

140 ty factors (including VPF), and reduction of VPF expression by tumor cells.

141 Sp1-dependent transcriptional regulation of VPF/VEGF expression and thus tumor angiogenesis.

142 The up-regulation of VPF/VEGF expression by Ras has been found to be through

143 on as a downstream step in PKC regulation of VPF/VEGF expression.

144 Sp1-dependent transcriptional regulation of VPF/VEGF.

145 Normally, release of VPF/ VEGF must be under strict control because it is som

146 To better define the role of VPF/VEGF in tumor biology, we screened tumorigenic lines

147 the loss of normal, controlled secretion of VPF/VEGF after damage to visceral epithelial cells could

148 bly, the Fc epsilonRI-dependent secretion of VPF/VEGF by either mouse or human mast cells can be sign

149 of HuR in order to regulate the stability of VPF/VEGF mRNA.

150 VHL not only inhibits the transcription of VPF/VEGF but also plays a significant role in decreasing

151 ay whereby Ras promotes the transcription of VPF/VEGF by activating protein kinase Czeta (PKCzeta).

152 ene c-Src in regulating the transcription of VPF/VEGF in breast cancer cell lines MCF-7 and MDA-MB 43

153 significantly inhibited the transcription of VPF/VEGF involving the transcription factor Sp1.

154 reversible in that subsequent withdrawal of VPF/VEGF returned cells to the senescent phenotype.

155 ant for the destabilizing function of VHL on VPF/VEGF mRNA.

156 sion in RCC cells that regularly overexpress VPF/VEGF.

157 Src kinase activity and thereby may prevent VPF/VEGF transcription.

158 r promoting angiogenesis, thereby preventing VPF/VEGF binding, receptor phosphorylation and subsequen

159 We now report that oral doxycycline prevents VPF/VEGF-induced vascular permeability, interleukin-2-in

160 L glioma cell-conditioned medium or purified VPF, and intracerebral vascular permeability induced by

161 ke growth factor receptor (IGF-IR) regulates VPF/VEGF expression.

162 Hypoxia often up-regulates VPF/VEGF expression further.

163 stigated the pathways by which VHL regulates VPF/VEGF expression.

164 Mouse mast cells release VPF/VEGF upon stimulation through Fcepsilon receptor I (

165 A23187; such mast cells can rapidly release VPF/VEGF, apparently from a preformed pool, and can then

166 hibition of protein kinase C (PKC) represses VPF/VEGF expression in RCC cells that regularly overexpr

167 or human mast cells can produce and secrete VPF/VEGF.

168 the mast cell, can be stimulated to secrete VPF/VEGF upon immunologically specific activation via a

169 Cells transfected with sense VPF/VEGF (V+) expressed and secreted large amounts of mo

170 e VHL (wt-VHL) gene product acts to suppress VPF/VEGF expression, which is overexpressed when wt-VHL

171 Immunoblots confirmed that VPF/VEGF induced tyrosine phosphorylation of several pro

172 These experiments demonstrate that VPF/VEGF promotes melanoma growth by stimulating angioge

173 significantly reduced in senescent EC, that VPF/VEGF modulates thymosin beta-10 expression, and that

174 We report here that VPF significantly enhances permeability in aortic endoth

175 explain these findings, we hypothesized that VPF increased the permeability of tumor blood vessels by

176 or cells in KS and angiosarcoma implies that VPF/VEGF may also have a direct effect on tumor cells.

177 nducing glomeruloid bodies and indicate that VPF/VEGF(164) is sufficient for their induction and nece

178 Our previous studies indicated that VPF is expressed early after infection and has a native

179 l vessels in and around tumors suggests that VPF/VEGF may be an important regulator of the edema and

180 To further characterize the VPF/VEGF-stimulated HUVEC proliferation and migration he

181 sels in vivo and have further elucidated the VPF/VEGF signaling cascade.

182 Other experiments further elucidated the VPF/VEGF signaling pathway, demonstrating phosphorylatio

183 ought to be mediated by other members of the VPF/VEGF family, namely, VEGF-C and VEGF-D.

184 Increased binding of Sp1 to the VPF/VEGF promoter has been observed when the cells were

185 lex with Sp1 and inhibits its binding to the VPF/VEGF promoter to prevent the transcriptional activat

186 ed the PKCzeta-induced binding of Sp1 to the VPF/VEGF promoter.

187 were observed when mesentery was exposed to VPF/VEGF in vitro, or when mesenteries were harvested fr

188 would engage in signaling steps that lead to VPF/VEGF overexpression.

189 acellular Ca(2+) mobilization in response to VPF/VEGF but have no effect on KDR and MAPK phosphorylat

190 merous microvessels are highly responsive to VPF/VEGF and that we found to express Flk-1 and Flt-1 se

191 Taken together, VPF/VEGF delayed the onset of senescence and also revers

192 Antisense-transfected VPF/VEGF (V-) cells expressed reduced constitutive VPF/V

193 Typically, VPF/VEGF-treated HDMEC could be cultured for at least 15

194 i.e., blocking the interactions between VEFG/VPF and endothelial cells or inhibiting VEGF/VPF synthes

195 s ligand, vascular permeability factor/VEGF (VPF/VEGF), arguably the most important angiogenic cytoki

196 educed by neutralization of endogenous VEGF/ VPF and suggest that angiogenesis and the maintenance of

197 Moreover, VEGF/ VPF expression was identified in 32 (97%) of 33 patholog

198 VEGF/VPF and positive controls (platelet-activating factor [P

199 VEGF/VPF double immunostaining and in situ hybridization demo

200 VEGF/VPF expression by cells of hypoxic tissues coincides wit

201 VEGF/VPF expression in the wall and/or plaque of medium to la

202 VEGF/VPF immunostaining among primary atherosclerotic lesions

203 VEGF/VPF increased IL-8 production in HBMECs through activati

204 VEGF/VPF may also serve as a local, endogenous regulator of l

205 VEGF/VPF produced a dose-dependent rise in NO concentration (

206 VEGF/VPF stimulates production of NO from rabbit and human EC

207 VEGF/VPF was detected immunohistochemically in sections of no

208 VEGF/VPF-induced permeability was significantly attenuated by

209 VEGF-secreted isoforms: VEGF/VPF(121), VEGF/VPF(145), and VEGF/VPF(165).

210 In addition, VEGF/VPF is a potent angiogenic factor.

211 dy (A4.6.1) (492 micrograms/ml) against VEGF/VPF or PBS (control).

212 Although VEGF/VPF expression was observed in areas of macrophage infil

213 itation analysis revealed that although VEGF/VPF induced IL-8 expression at the translational level i

214 orms: VEGF/VPF(121), VEGF/VPF(145), and VEGF/VPF(165).

215 e treated with a neutralizing antihuman VEGF/VPF antibody developed ascites and effusion lymphoma.

216 rrelation could be demonstrated between VEGF/VPF immunostaining and extent of vasa vasorum.

217 ressed the VEGF/VPF receptor Flt-1, but VEGF/VPF did not stimulate proliferation in these cells.

218 HL were found to produce mRNAs encoding VEGF/VPF, the glucose transporter GLUT1, and the platelet-der

219 VEGF/vascular permeability factor (VEGF/VPF or VEGF-A) is a pivotal driver of cancer angiogenesi

220 th factor/vascular permeability factor (VEGF/VPF) and basic fibroblast growth factor (bFGF) are expre

221 th factor/vascular permeability factor (VEGF/VPF) did not differ between 9L-neo and 9L-SF tumors.

222 th factor/vascular permeability factor (VEGF/VPF) is an endothelial-cell-specific mitogen; as such, i

223 h factor/ vascular permeability factor (VEGF/VPF) mRNA expression was determined by the Northern blot

224 th factor/vascular permeability factor (VEGF/VPF) released by neoplastic and/or host cells.

225 th factor/vascular permeability factor (VEGF/VPF), or in rats that were diabetic for 2, 4, 6, or 8 mo

226 or vascular endothelial growth factor (VEGF/VPF)-transfected MCF-7 breast carcinoma cells growing as

227 th factor/vascular permeability factor (VEGF/VPF).

228 th factor/vascular permeability factor (VEGF/VPF).

229 D45RO-positive cells as responsible for VEGF/VPF expression in such areas.

230 um to large vessels suggests a role for VEGF/VPF other than promoting angiogenesis.

231 evidence for the presence of functional VEGF/VPF receptors on quiescent endothelium of the adult rabb

232 Surprisingly, however, VEGF/VPF expression in normal and/or atherosclerotic vessels

233 permeability independent of changes in VEGF/VPF expression.

234 methyl ester (20 mg/kg) did not inhibit VEGF/VPF-induced permeability.

235 s of the HBMEC monolayer also inhibited VEGF/VPF-induced permeability and the cytoskeletal rearrangem

236 VPF and endothelial cells or inhibiting VEGF/VPF synthesis in solid tumors causes dramatic reduction

237 amplified the 3 VEGF-secreted isoforms: VEGF/VPF(121), VEGF/VPF(145), and VEGF/VPF(165).

238 ouble immunostaining failed to localize VEGF/VPF to macrophages in these foci; instead, double immuno

239 stimulatory effect of 10 micrograms/mL VEGF/VPF.

240 ulated by addition of 2.5 micrograms/mL VEGF/VPF.

241 human coronary arteries for evidence of VEGF/VPF expression.

242 this study, we investigated the role of VEGF/VPF in breast cancer metastasis to the brain.

243 dered central to the documented role of VEGF/VPF in promoting angiogenesis.

244 were consistent with the measurement of VEGF/VPF in that the VEGF/VPF mRNA level was lower in the liv

245 f tumor vessels require the presence of VEGF/VPF in the tissue microenvironment.

246 that putative maintenance functions of VEGF/VPF may include regulation of baseline synthesis and/or

247 its effects via paracrine induction of VEGF/VPF receptors in ECs.

248 onary arterial specimens; the extent of VEGF/VPF staining was graded as moderate to strong in 21 of t

249 that IL-8 mRNA was maximal after 1 h of VEGF/VPF treatment of the cells.

250 increased [NO] after administration of VEGF/VPF was slower, reaching a maximum value after 8 minutes

251 tacyclin produced by the interaction of VEGF/VPF with its Flk-1/KDR/VEGF-R2 receptor as mediators of

252 To examine this role of VEGF/VPF, we used a Transwell culture system of the human bra

253 say) to study the putative mediators of VEGF/VPF-induced permeability.

254 -1/KDR/VEGF-R2 receptor as mediators of VEGF/VPF-induced vascular permeability.

255 e the pleura and express high levels of VEGF/VPF.

256 titute the principal cellular source of VEGF/VPF.

257 Six hours postinjection, VEGF/VPF-treated rats exhibited a threefold increase in BRB P

258 findings thus establish that postnatal VEGF/VPF expression is a feature of normal human arteries and

259 ors genistein or herbimycin A prevented VEGF/VPF-induced permeability.

260 mal or neoplastic, not only can produce VEGF/VPF, but can also modulate its effects via paracrine ind

261 In restenotic specimens, VEGF/VPF immunostaining was more prominently cellular, partic

262 These data suggest that VEGF/VPF can modulate the TM of tumor cells by regulating the

263 Interestingly, we also observed that VEGF/VPF induced interleukin-8 (IL-8) expression in HBMECs an

264 is increased migration, indicating that VEGF/VPF induced the functional expression of IL-8 protein in

265 ata demonstrate for the first time that VEGF/VPF induces IL-8 expression in HBMECs and contributes to

266 These results demonstrate that VEGF/VPF is critical to BCBL-1 growth as effusion lymphoma in

267 More recent evidence suggests that VEGF/VPF may also serve a "maintenance" function, modulating

268 together, these findings indicate that VEGF/VPF might contribute to breast cancer metastasis by enha

269 We observed that VEGF/VPF significantly increased the penetration of the highl

270 In vitro studies confirmed that VEGF/VPF stimulates synthesis of NO and prostaglandin metabol

271 usion lymphoma in mice and suggest that VEGF/VPF stimulation of vascular permeability may be critical

272 We hypothesized that VEGF/VPF, having potent vascular permeability activity, may s

273 the measurement of VEGF/VPF in that the VEGF/VPF mRNA level was lower in the liver tumor than that in

274 eatment of the HBMEC monolayer with the VEGF/VPF receptor (KDR/Flk-1) inhibitor, SU-1498, and the cal

275 Two of the PEL cell lines expressed the VEGF/VPF receptor Flt-1, but VEGF/VPF did not stimulate proli

276 Supernatants of the VEGF/VPF-treated HBMECs significantly increased neutrophil mi

277 reover, this property appears unique to VEGF/VPF among angiogenic cytokines.

278 The signaling pathways that underlie VEGF/VPF-induced permeability are not well defined.

279 To determine whether VEGF/VPF is directly involved in chemokine secretion, we anal

280 The mechanism by which VEGF/VPF increases vascular permeability (VP), however, has r

281 sought to determine the extent to which VEGF/VPF may stimulate the release of NO from normal ECs.

282 increase in permeability observed with VEGF/VPF.

283 lation pathway, we also investigated whether VPF/VEGF facilitates thrombin cleavage of OPN in vivo.

284 Early passage HDMEC cultured with or without VPF/VEGF overexpressed 9 and underexpressed 6 genes in c