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/VEGF acts selectively on the vascular endothelium to

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

4 VPF/VEGF induced dermal microvascular EC expression of m

5 VPF/VEGF induces vascular hyperpermeability, cell divisi

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

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

8 VPF/VEGF stimulates endothelial cell growth and increase

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

27 -1 pancreatic carcinoma cells, Sp1-dependent VPF/VEGF transcription is controlled by IGF-1R signaling

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

60 dentified as a vascular permeability factor (VPF).

61 eted cytokine, vascular permeability factor (VPF).

62 t described as vascular permeability factor (VPF).

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

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

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

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

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

68 zing the vaccinia virus processivity factor (VPF).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

90 1, p16 and p27) was significantly reduced in VPF/VEGF-treated cells but p53 expression was not signif

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

107 Like VPF, histamine and serotonin also stimulated ferritin ex

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

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

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

111 2 cells stably with sense or antisense mouse VPF/VEGF cDNA or with vector alone.

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

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

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

115 ere relatively impermeable in the absence of VPF stimulation.

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

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

118 permeabilizing and angiogenic activities of VPF/VEGF.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

136 Sp1-dependent transcriptional regulation of VPF/VEGF.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

191 VEGF/VPF double immunostaining and in situ hybridization demo

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

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

194 VEGF/VPF immunostaining among primary atherosclerotic lesions

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

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

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

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

199 VEGF/VPF was detected immunohistochemically in sections of no

200 VEGF/VPF-induced permeability was significantly attenuated by

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

225 permeability independent of changes in VEGF/VPF expression.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

246 -1/KDR/VEGF-R2 receptor as mediators of VEGF/VPF-induced vascular permeability.

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

248 titute the principal cellular source of VEGF/VPF.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

274 increase in permeability observed with VEGF/VPF.

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

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