ライフサイエンスコーパス: VEGF-C

1 VEGF C-producing uNK cells support endovascular processe

2 VEGF-C and VEGF-A increased [Ca2+]i by 15% and 39%, resp

3 VEGF-C and VEGF-D are secreted glycoproteins that induce

4 VEGF-C and VEGF-D were identified as lymphangiogenic gro

5 VEGF-C and VEGF-D were thought to exhibit similar bioact

6 VEGF-C and VEGFR-3 expressions were examined with immuno

7 VEGF-C blockade, through administration of a VEGF-C bloc

8 VEGF-C directly stimulated RANKL-mediated bone resorptio

9 VEGF-C effects on intracellular calcium ([Ca2+]i) were m

10 VEGF-C effects on trans-endothelial electrical resistanc

11 VEGF-C expression was demonstrated to be markedly upregu

12 VEGF-C functions in both physiological and pathological

13 VEGF-C increased GEnC monolayer integrity and increased

14 VEGF-C increased the survival of prostate cancer cells d

15 VEGF-C induced lung lymphangiogenesis and promoted intra

16 VEGF-C is therefore a good target to slow or even preven

17 VEGF-C loss did not disrupt the generation of primitive

18 VEGF-C overexpression in tracheal allografts induced epi

19 VEGF-C phosphorylated VEGFR-2 but not VEGFR-3, myosin li

20 VEGF-C reduced labeled albumin flux by 32.8%.

21 VEGF-C signaling through VEGFR-3 promotes lymphangiogene

22 VEGF-C was blocked in the angiogenesis and transplant mo

23 VEGF-C, expressed mainly in vascular smooth muscle cells

24 VEGF-C-dependent protection was observed in combination

25 VEGF-C-induced LAM cell proliferation was in part a resu

26 VEGF-C-mediated bone resorption was abolished in Src(-/-

27 VEGF-C-mediated Erk1/2 phosphorylation was inhibited in

28 VEGF-C/R-2 complex in the cytoplasm of VEGF-A-treated en

29 iated viral vector-mediated soluble VEGFR-3 (VEGF-C/D Trap) completely blocked lymphangiogenesis, sho

30 MSCs showed migratory activity along a VEGF-C gradient, which was enhanced by VEGF-C conditioni

31 loprotease with thrombospondin motifs-3 as a VEGF-C-activating protease and reveal a novel type of re

32 In a transgenic mouse model expressing a VEGF-C/D trap and displaying complete aplasia of the dur

33 VEGF-C blockade, through administration of a VEGF-C blocking monoclonal antibody, suppresses corneal

34 ammary tumor cells stably transfected with a VEGF-C siRNA vector were significantly lower compared wi

35 Vascular endothelial growth factor-A, VEGF-C, and VEGF-R2 mRNA expression were increased in VE

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

37 We found that in contrast to VEGF-A, VEGF-C does not increase the growth of primary tumors, b

38 acterized by higher plasma levels of VEGF-A, VEGF-C, and Ang2 compared with the other patients.

39 iferation and decreased secretion of VEGF-A, VEGF-C, and basic fibroblast growth factor.

40 ure system reinforced by addition of VEGF-A, VEGF-C, and EGF most efficiently generated LECs, which w

41 ed reduced expression of KLF2, KLF4, VEGF-A, VEGF-C, and FGFR3 and elevated expression of p57.

42 as well as VEGF signaling molecules VEGF-A, VEGF-C, and VEGF-D.

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

44 of TNF-alpha, IL-1 alpha, IL-1 beta, VEGF-A, VEGF-C, and VEGFR2.

45 Plasma concentrations of VEGF-A, VEGF-C, Ang1, and Ang2 were higher in patients with C1-I

46 2 KLF proteins cooperate to regulate VEGF-A, VEGF-C, FGFR3, and p57 by binding to the regulatory regi

47 showed that the Gibbs free energy of VEGF-A, VEGF-C, or VEGF-E binding to D23 or the full-length ECD

48 VEGF-A, VEGF-C, TGF-beta1, and Ang-2 all stimulated human aorta

49 ctor, soluble TIE-1, soluble VEGFR1, VEGF-A, VEGF-C, VEGF-D, VEGF-A isoform 121, bone morphogenetic p

50 vascular endothelial growth factor [VEGF]-A, VEGF-C, soluble VEGF receptor [sVEGFR]-3, and placental

51 ndicating that SIX1 acts through additional, VEGF-C-independent pathways.

52 Intranodally injected adenoviral VEGF-C and adenoviral vector encoding control gene LacZ

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

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

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

56 n which galectin-8-dependent crosstalk among VEGF-C, podoplanin and integrin pathways plays a key rol

57 By analyzing VEGF-C produced by CCBE1-transfected cells, we found tha

58 Mean plasma VEGF-A (P = .002) and VEGF-C (P = .01) levels decreased 24 hours postinfusion,

59 , the reciprocal interplay between FGF-2 and VEGF-C collaboratively stimulated tumor growth, angiogen

60 Here we show that FGF-2 and VEGF-C, two lymphangiogenic factors, collaboratively pro

61 intervention and targeting of the FGF-2- and VEGF-C-induced angiogenic and lymphangiogenic synergism

62 phatic tip cell formation in both FGF-2- and VEGF-C-induced lymphangiogenesis.

63 Baseline levels of sVEGFR-3 and VEGF-C may have potential utility as biomarkers of clini

64 Lower baseline levels of sVEGFR-3 and VEGF-C were associated with longer PFS and ORR.

65 nd alpha5beta1 curtails both galectin-8- and VEGF-C-mediated LEC sprouting.

66 ption factor highly implicated in VEGF-A and VEGF-C gene regulation.

67 In vitro FRS2alpha regulates VEGF-A and VEGF-C-dependent activation of extracellular signal-regu

68 lar endothelial growth factor-A (VEGF-A) and VEGF-C (cancer growth regulators) were measured after 82

69 lar endothelial growth factor A (VEGF-A) and VEGF-C gene expression as early as 30 min postinfection

70 is the major inducer of RalA activation and VEGF-C synthesis.

71 s (e.g. placental growth factor, VEGF-B, and VEGF-C), which may play a role in angiogenesis.

72 VEGFR-3 in tissue sections and culture, and VEGF-C increased trans-endothelial electrical resistance

73 oietin (Ang)-1, Ang-2, interferon-gamma, and VEGF-C also disrupted VSMC integrity with an Ang-2 inhib

74 at the maintenance of lymphatic identity and VEGF-C-induced lymphangiogenic activity, including cell

75 nsitive to rapamycin, an mTOR inhibitor, and VEGF-C addition.

76 uppressed the enhanced lymphangiogenesis and VEGF-C expression associated with fibrosis in a rat mode

77 2 pathway expressed decreased M2 markers and VEGF-C production and exhibited aberrant lymphangiogenes

78 responses during the development of OAD, and VEGF-C/VEGFR-3 signaling modulated innate and adaptive i

79 certain other HIF-responsive genes (PHD3 and VEGF-C) are induced following IFN-alpha and/or IFN-gamma

80 is by demonstrating coexpression of SIX1 and VEGF-C in human breast cancer.

81 vascular endothelial growth factors VEGF and VEGF-C down-regulation in cancer cells appeared insuffic

82 t significant side effects, whereas VEGF and VEGF-C incited growth of aberrant vessels, severe edema,

83 scular endothelial growth factor (VEGF), and VEGF-C in diluted serum.

84 Osteoclasts express VEGFR3, and VEGF-C stimulated Src phosphorylation in osteoclasts.

85 vWF and VEGF-C expression decreased in BDL Kit(W-sh) mice.

86 Anti-VEGF-C and sVEGFR3 significantly decreased graft lymphan

87 VEGF-trap (72%), anti-VEGF-C (25%), and sVEGFR-3 (11%) all significantly impro

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

89 significantly more effective than both anti-VEGF-C (P < 0.05) and sVEGFR-3 (P < 0.05).

90 ant model using neutralizing monoclonal anti-VEGF-C (VGX-100) by intraperitoneal injection.

91 long-term graft survival as compared to anti-VEGF-C and sVEGFR-3, but all approaches improve survival

92 endothelial growth factor (VEGF)-trap, anti-VEGF-C, sVEGFR-3, or no treatment, beginning at the time

93 ignant tumors release growth factors such as VEGF-C to induce lymphatic vessel expansion (lymphangiog

94 ced cell apoptosis, indicative of autonomous VEGF-C autocrine signaling essential for LEC survival.

95 ssociates with fibrosis through the TGF-beta-VEGF-C pathway.

96 GFR-3 suppresses hemangiogenesis by blocking VEGF-C-induced phosphorylation of VEGFR-2.

97 podocytes direct GEnC behavior through both VEGF-C and VEGF-A.

98 We show that cytoprotection by VEGF C can be related to induction of the TAP-1 expressi

99 the androgen receptor co-activator BAG-1L by VEGF-C, suggesting the involvement of this growth factor

100 e proliferation in vitro was not affected by VEGF-C or VEGF-D, indicating indirect effects of sVEGFR-

101 overexpression in mouse airways is driven by VEGF-C/D from macrophages, but not neutrophils, recruite

102 ong a VEGF-C gradient, which was enhanced by VEGF-C conditioning.

103 and suppressing lymphangiogenesis induced by VEGF-C. sVEGFR-3 knockdown leads to lymphangiogenesis an

104 uting responses, including those mediated by VEGF-C, remains to be examined.

105 Vascular endothelial growth factor C (VEGF-C) is a major driver of lymphangiogenesis in embryo

106 oviral vascular endothelial growth factor C (VEGF-C) was administered intranodally or perinodally.

107 ligand vascular endothelial growth factor C (VEGF-C), is a major mediator of lymphangiogenesis.

108 ogenic vascular endothelial growth factor C (VEGF-C), its receptor VEGFR-3, and lymphangiogenesis dur

109 xpress vascular endothelial growth factor-C (VEGF-C) and green fluorescent protein specifically in th

110 ion of vascular endothelial growth factor-C (VEGF-C) and its cognate receptor VEGF receptor-3 (VEGFR3

111 uch as vascular endothelial growth factor-C (VEGF-C) and VEGF-A, induce lymphatic vessel expression o

112 sis by vascular endothelial growth factor-C (VEGF-C) at the secondary site, in the lung, facilitates

113 ase in vascular endothelial growth factor-C (VEGF-C) expression in human prostate cancer cells after

114 local vascular endothelial growth factor-C (VEGF-C) expression, reduced numbers of VEGF-C(+) cells,

115 th the vascular endothelial growth factor-C (VEGF-C) growth factor signaling pathway, which is critic

116 sis by vascular endothelial growth factor-C (VEGF-C) has been shown to play an important role in prom

117 diator vascular endothelial growth factor-C (VEGF-C) in human dialysate effluents, peritoneal tissues

118 ion of vascular endothelial growth factor-C (VEGF-C) in metastatic prostate cancer.

119 human vascular endothelial growth factor-C (VEGF-C) in PC-3 cells reduced intratumoral lymphatics by

120 rce of vascular endothelial growth factor-C (VEGF-C) in the tumor microenvironment.

121 Vascular endothelial growth factor-C (VEGF-C) is a secreted growth factor essential for lympha

122 d that vascular endothelial growth factor-C (VEGF-C) is one such target gene of NKX3.1.

123 Both vascular endothelial growth factor-C (VEGF-C) ligand trap (sVEGFR-3) and antibody directed aga

124 nce of vascular endothelial growth factor-C (VEGF-C) to the lymph node metastasis seen in human prost

125 uch as vascular endothelial growth factor-C (VEGF-C), would limit peritumor hyperplasia, and decrease

126 phatic vascular endothelial growth factor-C (VEGF-C).

127 ), and vascular endothelial growth factor-C (VEGF-C).

128 actor (vascular endothelial growth factor-C [VEGF-C]) can promote lymphatic growth and maturation in

129 arker (Vascular Endothelial Growth Factor-C, VEGF-C) through the use of antibody-modified AuNPs and n

130 and the D7 interaction (Arg737) compromised VEGF-C induced VEGFR-3 activation.

131 vascular endothelial growth factor-C and -D (VEGF-C, -D).

132 nd is likely driven by myoepithelial-derived VEGF-C and/or VEGF-D.

133 nct signaling mechanisms (e.g. tumor-derived VEGF-C promoted expression of the prostaglandin biosynth

134 Dialysate VEGF-C concentration correlated positively with the dial

135 ion, enhanced sprouting efficiency, elevated VEGF-C expression and COX2 expression, shorter doubling

136 ew strategy for the liberation of endogenous VEGF-C and the prevention of lymphatic regression.

137 This response can be reversed by exogenous VEGF C.

138 sentinel lymph nodes, tumors that expressed VEGF-C were more likely to metastasize to additional org

139 Metastases expressing VEGF-C were tightly associated with the airways, in cont

140 mined that the lymphangiogenic growth factor VEGF-C and its receptor, VEGFR-3, are essential for SC d

141 viral induction of prolymphangiogenic factor VEGF-C provides marked protection against the developmen

142 anscription of the prolymphangiogenic factor VEGF-C, and this was required for lymphangiogenesis and

143 oclasts secrete the lymphatic growth factor, VEGF-C, to increase their resorptive activity.

144 The prolymphangiogenic growth factor, VEGF-C, was elevated in atherosclerotic aortic walls.

145 atic endothelium to VEGFR-3 binding factors, VEGF-C and VEGF-D, ultimately resulting in robust lympha

146 Upregulation of WDFY-1 following VEGF-C or NRP-2 depletion contributes to cytotoxic drug-

147 acted in synergy with the loss of NKX3.1 for VEGF-C transcription.

148 e between AuNPs with attached antibodies for VEGF-C and antigen-conjugated particles.

149 expression of neuropilin-2, a coreceptor for VEGF-C.

150 udied in detail for VEGFR3, the receptor for VEGF-C.

151 These results reveal an unexpected role for VEGF-C, a major lymphangiogenic growth factor, in the tr

152 (NPC) was increased in CD fetal hippocampus VEGF C (Vegfc), 2.0-fold, p < 0.01 vs. CT and angiopoiet

153 ing a direct mechanistic explanation for how VEGF-C expression is upregulated in breast cancer, resul

154 However, VEGF-C activation of LEC-specific VEGFR3 receptors block

155 -like qualities of this canal: they identify VEGF-C as a potential therapeutic for glaucoma and sugge

156 ymphatic-like phenotype of the SC, implicate VEGF-C and VEGFR-3 as critical regulators of SC lymphang

157 urce of prolymphangiogenic stimuli including VEGF-C and VEGF-D with temporally regulated expression l

158 , forced expression of C/EBP-delta increased VEGF-C and VEGFR3 expression in cultured LECs.

159 apping mechanism explains, despite increased VEGF-C in the atherosclerotic aortas, how adventitial ly

160 Despite increased VEGF-C, we found that adventitial lymphatics regress dur

161 -kDa form of VEGF-C, which induces increased VEGF-C receptor signaling.

162 cer, and the loss of NKX3.1 led to increased VEGF-C expression.

163 activity totally blocked CEBP-delta-induced VEGF-C and VEGFR3 expression in LECs.

164 RANKL-induced VEGF-C expression was reduced in NF-kappaBp50(-/-)/p52(-

165 NKX3.1 inhibited VEGF-C expression in prostate cancer, and the loss of NK

166 FR-sema3C also inhibited VEGF-C-induced phosphorylation of VEGFR-3, ERK1/2, and A

167 heparan sulfate chain biosynthesis inhibited VEGF-C-mediated Erk1/2 activation and abrogated VEGFR-3

168 nC and investigate the effects of the ligand VEGF-C.

169 sine kinase that is activated by its ligands VEGF-C and VEGF-D.

170 ngiogenic (VEGF-A165b ) and lymphangiogenic (VEGF-C) factors were evaluated by ELISA.

171 also inhibited phosphorylation of the major VEGF-C receptor VEGFR-3 upon VEGF-C stimulation.

172 responding part of the alpha-helix in mature VEGF-C did not influence binding to either VEGFR-2 or VE

173 Consistent with this mechanism, VEGF-C immunoreactivity was present in some Aif1/Iba1-im

174 Mechanistically, VEGF-C-induced lymphangiogenesis is significantly reduce

175 These findings indicate that eNOS mediates VEGF-C-induced lymphangiogenesis and, consequently, play

176 In addition, FGF2 but not VEGF-C-induced in vivo lymphangiogenesis, was also inhib

177 ibitor library and identify three novel Nrp2/VEGF-C binding inhibitors from the National Institutes o

178 Moreover, the ability of VEGF-C and rapamycin to normalize LEC responses suggests

179 However, the ability of VEGF-C to enhance sustainable, functional lymphatic grow

180 163(+)/CD68(+)/VEGFC(+) cells and absence of VEGF-C expression by CD3(+) or CD11C(+) cells suggested

181 ed and matured in the presence or absence of VEGF-C.

182 enhanced the pro-lymphangiogenic actions of VEGF-C, at least in part by directly stimulating express

183 osis binds to and diminishes the activity of VEGF-C.

184 he node, whereas perinodal administration of VEGF-C did not have this adverse effect.

185 athologic conditions; however, alteration of VEGF-C/VEGFR3 signaling did not modulate SC integrity an

186 ogated VEGFR-3 receptor-dependent binding of VEGF-C to the lymphatic endothelial surface.

187 tone deacetylase 1 acted as a corepressor of VEGF-C expression along with NKX3.1.

188 Delivery of VEGF-C into the adult eye resulted in sprouting, prolife

189 ry were necessary for selective detection of VEGF-C.

190 By contrast, no difference of VEGF-C in tumor tissues and bone marrow was observed bet

191 be a microplate-based assay for discovery of VEGF-C/Nrp2 inhibitors.

192 The effect of VEGF-C signaling on osteoclast function was determined b

193 Here, we have studied the effects of VEGF-C and VEGF-D on tumor development in the murine mul

194 Conversely, an excess of VEGF-C induced meningeal lymphangiogenesis.

195 RANKL increased the expression of VEGF-C but not of other VEGFs in osteoclasts and their p

196 The mRNA and protein expression of VEGF-C in murine mammary tumor cells stably transfected

197 Interestingly, the higher expression of VEGF-C in prostate cancer is also correlated with lymph

198 esothelial cell and macrophage expression of VEGF-C increased in the peritoneal membranes of patients

199 lls, TGF-beta1 upregulated the expression of VEGF-C mRNA and protein, and this upregulation was suppr

200 Forced expression of VEGF-C, but not recombinant VEGF-C, rescued the knockdow

201 LCM confirmed the increased expression of VEGF-C, the SCC inflammatory infiltrate.

202 ic development, due to reduced expression of VEGF-C.

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

204 he otherwise poorly active 29/31-kDa form of VEGF-C by the A disintegrin and metalloprotease with thr

205 giogenesis with VEGF-C156S, a mutant form of VEGF-C with selective VEGFR-3 binding, alleviates an est

206 e, resulting in the mature 21/23-kDa form of VEGF-C, which induces increased VEGF-C receptor signalin

207 we unveil a novel hematopoietic function of VEGF-C in fetal erythropoiesis.

208 tinctly different from the known function of VEGF-C in inducing lymphangiogenesis.

209 To determine the function of VEGF-C in maturation of antigen-presenting cells (APCs),

210 ngs suggest a novel and distinct function of VEGF-C in protecting cancer cells from stress-induced ce

211 The protective function of VEGF-C was meditated by the so-called resolving MPhis du

212 ttenuates peritumor lymphatic hyperplasia of VEGF-C-overexpressing T241 fibrosarcomas and decreases t

213 The functional importance of VEGF-C was investigated by adenovirus-mediated overexpre

214 n of VEGF-C (AdVEGF-C), and by inhibition of VEGF-C activity with VEGFR-3-Ig (AdVEGFR-3-Ig).

215 In contrast, inhibition of VEGF-C activity with VEGFR-3-Ig inhibited lymphangiogene

216 In summary, our data show that inhibition of VEGF-C expression using siRNA-mediated gene silencing ve

217 poiesis, whereas the possible involvement of VEGF-C in hematopoiesis is unknown.

218 angitic carcinomatosis showed high levels of VEGF-C expression in cancer cells.

219 lammatory macrophages produce high levels of VEGF-C to coordinately activate VEGFR3.

220 patients with UFF expressed higher levels of VEGF-C, lymphatic endothelial hyaluronan receptor-1 (LYV

221 ity in adult periods through manipulation of VEGF-C-VEGFR3 signaling.

222 rom paws to popliteal LNs, and the number of VEGF-C-expressing CD11b+ myeloid cells in popliteal LNs.

223 or-C (VEGF-C) expression, reduced numbers of VEGF-C(+) cells, and reductions in inflammatory lymphang

224 ted by adenovirus-mediated overexpression of VEGF-C (AdVEGF-C), and by inhibition of VEGF-C activity

225 Unexpectedly, perinatal overexpression of VEGF-C in the respiratory epithelium led to a condition

226 RT-PCR confirmed the presence of VEGF-C in skin immediately adjacent to SCC.

227 Therefore, regulation of VEGF-C expression by NKX3.1 provides a possible mechanis

228 These findings indicate an important role of VEGF-C-induced lymph node lymphangiogenesis in the promo

229 nimal role in immunopathology as a source of VEGF-C.

230 Here we analyzed the crystal structures of VEGF-C in complex with VEGFR-3 domains D1-2 and of the V

231 TGF-beta1-induced upregulation of VEGF-C mRNA expression in cultured HPMCs correlated with

232 Our results support the use of VEGF-C/VEGF-D-blocking agents not only to inhibit metast

233 trolled transactivator/tetracycline operator-VEGF-C double-transgenic mice during a critical period f

234 ters of lymphatic vessels draining Ang-4- or VEGF-C (positive control)-expressing tumors increased to

235 FR-3-specific ligands than that by VEGF-A or VEGF-C.

236 that, whereas CCBE1 itself does not process VEGF-C, it promotes proteolytic cleavage of the otherwis

237 Peripheral blood NK cells fail to produce VEGF C and remain cytotoxic.

238 us cell carcinoma secrete prolymphangiogenic VEGF-C.

239 xposed to lymph-inductive media and purified VEGF-C.

240 ed expression of VEGF-C, but not recombinant VEGF-C, rescued the knockdown of C/EBP-delta-induced cel

241 rthermore, a single injection of recombinant VEGF-C induced SC growth and was associated with trend t

242 dst1 gene-targeted mice demonstrated reduced VEGF-C- and FGF-2-mediated sprouting in collagen matrix.

243 rowth factor-A (VEGF-A) surprisingly reduced VEGF-C in the supernatant of blood vessel endothelial ce

244 osteoclasts and their precursors to release VEGF-C through an NF-kappaB-dependent mechanism, indicat

245 in which CA stem development first requires VEGF-C to stimulate vessel growth around the outflow tra

246 Western blots and immunostaining revealed VEGF-C and VEGFR-3 expression in CNV lesions, mainly in

247 s.c. tumors, indicating that tumor-secreted VEGF-C is necessary for lymphangiogenesis.

248 agonist of lymphangiogenesis by sequestering VEGF-C.

249 l for corneal alymphaticity, by sequestering VEGF-C. sVEGFR-3 binds and sequesters VEGF-C, thereby bl

250 tering VEGF-C. sVEGFR-3 binds and sequesters VEGF-C, thereby blocking signaling through VEGFR-3 and s

251 ical significance of this prometastatic SIX1/VEGF-C axis by demonstrating coexpression of SIX1 and VE

252 f squamous cell carcinoma by using a soluble VEGF-C/VEGF-D inhibitor.

253 ations, transgenic mice expressing a soluble VEGF-C/VEGF-D receptor (sVEGFR-3) in the skin developed

254 These data suggest VEGF-C as a potentially important target in corneal tran

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

256 We demonstrate that VEGF-C binds to heparan sulfate purified from primary ly

257 e, using murine models, we demonstrated that VEGF-C-deficient hearts have severely hypoplastic peritr

258 We have discovered that VEGF-C acts directly on prostate cancer cells to protect

259 mouse mammary carcinoma model, we found that VEGF-C was not sufficient to mediate all the metastatic

260 We show here that VEGF-C/PI3Kalpha-driven remodeling of lymph nodes promot

261 The findings indicate that VEGF-C overexpression can induce pulmonary lymphangiecta

262 These findings indicate that VEGF-C/VEGF-D are involved in shaping the inflammatory t

263 -kappaB-dependent mechanism, indicating that VEGF-C is a new RANKL target gene in osteoclasts and fun

264 We observed that VEGF-C is widely expressed in the outflow tract, while c

265 metastasis models in nude mice, we show that VEGF-C expression by tumor cells altered the pattern of

266 These data show that VEGF-C promotes late steps of the metastatic process and

267 n by CD3(+) or CD11C(+) cells suggested that VEGF-C is derived from tumor-associated macrophages.

268 silencing of TAP-1 expression abolished the VEGF C-imparted protection.

269 N1b1b2 with Tuftsin, a peptide mimic of the VEGF C terminus, reveals the site of interaction with th

270 The VEGF-C receptors VEGFR3 and VEGFR2 are required for embr

271 The VEGF-C/VEGFR-3 and VEGF-A/VEGF-R2 signaling pathways are

272 ether, these data suggest a link between the VEGF-C/NRP-2 axis and cancer cell survival despite the p

273 ed bone resorption, which was reduced by the VEGF-C-specific receptor blocker, VEGFR3:Fc.

274 uropilin-2 was found to be essential for the VEGF-C-mediated AKT-1 activation.

275 s of the metastatic process and identify the VEGF-C/VEGF receptor-3 pathway as the target not only fo

276 A structural model of the VEGF-C/VEGFR-3 D1-7 complex derived from small-angle X-r

277 We have found that the VEGF-C/NRP-2 axis is involved in the activation of autop

278 Moreover, we found that the VEGF-C/VEGFR3 pathway regulates macrophage (MPhi) plasti

279 findings that alpha9beta1 directly binds to VEGF-C and -D and contributes to lymphangiogenesis, thes

280 RalA activation leads to VEGF-C upregulation.

281 d increased [Ca2+]i, which may be related to VEGF-C-S particular receptor binding and phosphorylation

282 only lymphatic vessel growth in response to VEGF-C could be appreciated.

283 lymphatic endothelial Erk1/2 in response to VEGF-C is reduced by interference with heparin or pretre

284 c endothelia, and scratch-assay responses to VEGF-C and FGF-2 were reduced in Ndst1-deficient cells.

285 -based growth and proliferation responses to VEGF-C.

286 increased endothelial cell responsiveness to VEGF-C, promoting endothelial cell survival and morpholo

287 Migratory activity toward VEGF-C in vitro suggests homing capability in vivo.

288 families of cell surface receptors transduce VEGF-C signals: neuropilin-2 (Nrp2) and VEGF-receptor (V

289 Furthermore, we identified two VEGF-C/NRP-2-regulated genes, LAMP-2 and WDFY-1, that ha

290 on of the major VEGF-C receptor VEGFR-3 upon VEGF-C stimulation.

291 sis induced by adeno-associated viral vector-VEGF-C.

292 enic vessels and away from exogenous GFs was VEGF-C dependent.

293 hus-associated lymphoid tissue (BALT), where VEGF-C-producing cells were scattered in T-cell zones.

294 PlGF levels significantly increased whereas VEGF-C and sVEGFR-3 levels decreased with sunitinib trea

295 ector were significantly lower compared with VEGF-C-control vector-transfected cells.

296 tanding functional differences compared with VEGF-C.

297 rection of defective lymphatic function with VEGF-C has potential as a therapeutic strategy for IBD.

298 s on therapeutic manipulation of the SC with VEGF-C in glaucoma treatment.

299 Treatment with VEGF-C alone also induced Prox-1 expression in the BEC-T

300 ng both receptors together or by withdrawing VEGF-C.