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-D are secreted glycoproteins that induce

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

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

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

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

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

8 VEGF-C expression was demonstrated to be markedly upregu

9 VEGF-C functions in both physiological and pathological

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

11 VEGF-C induced lung lymphangiogenesis and promoted intra

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

13 VEGF-C not only can serve as a diagnostic biomarker but

14 VEGF-C overexpression in tracheal allografts induced epi

15 VEGF-C signaling through VEGFR-3 promotes lymphangiogene

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

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

18 VEGF-C-dependent protection was observed in combination

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

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

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

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

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

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

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

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

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

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

29 0 fg/mL for DSG3, and 0.20 fg/mL for VEGF-A, VEGF-C and beta-Tub.

30 We found a significant increase of VEGF-A, VEGF-C, and Ang1 levels in U-HAE patients compared to co

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

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

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

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

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

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

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

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

39 2 KLF proteins cooperate to regulate VEGF-A, VEGF-C, FGFR3, and p57 by binding to the regulatory regi

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

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

42 upregulation of pro(lymph)angiogenic VEGF-A, VEGF-C, VEGF-D and infiltration of macrophages.

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

44 AAV8-VEGF-C injection significantly increased meningeal lymph

45 8-vascular endothelial growth factor C (AAV8-VEGF-C) was injected into the cisterna magna of HE rats

46 Furthermore, AAV8-VEGF-C decreased microglia activation (P < .001) and neu

47 cathepsin D as a protease that can activate VEGF-C as well as VEGF-D.

48 KLK3 is the third protease shown to activate VEGF-C.

49 KLK3 activated VEGF-C specifically and efficiently through cleavage at

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

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

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

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

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

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

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

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

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

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

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

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

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

63 t in increasing the expression of VEGF-A and VEGF-C via targeting the 3'UTR of mRNAs at a post-transc

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

65 ar endothelial growth factor A (VEGF-A), and VEGF-C.

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

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

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

69 del extensively after spinal cord injury and VEGF-C-induced vertebral lymphangiogenesis exacerbates t

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

71 2 pathway expressed decreased M2 markers and VEGF-C production and exhibited aberrant lymphangiogenes

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

89 cells infiltration, indicating that blocking VEGF-C signaling can reduce local chronic inflammation a

90 VEGF-A showed high in-cell expression, but VEGF-C had low levels inside cells.

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

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

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

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

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

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

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

98 ion of vascular endothelial growth factor C (VEGF-C) promotes enhanced priming of CD8 T cells in the

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

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

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

102 Vascular endothelial growth factor-C (VEGF-C) acts primarily on endothelial cells, but also on

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

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

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

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

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

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

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

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

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

112 X1 and vascular endothelial growth factor-C (VEGF-C) signaling.

113 GF-A), vascular endothelial growth factor-C (VEGF-C) were positive controls overexpressed into the HN

114 on for vascular endothelial growth factor-C (VEGF-C), that of maintaining the integrity of the BM per

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

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

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

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

119 Vegfc in club cell secretory protein (CCSP)/VEGF-C mice reduced macrophage accumulation and fibrosis

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

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

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

123 We detected VEGF-C in seminal plasma, and sperm liquefaction occurre

124 Dialysate VEGF-C concentration correlated positively with the dial

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

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

127 This response can be reversed by exogenous VEGF C.

128 Exogenous VEGF-C expanded the lymphatic population in explanted mo

129 sfection of an mRNA construct that expresses VEGF-C works synergistically with checkpoint blockade th

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

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

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

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

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

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

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

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

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

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

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

141 More importantly, we show that functional VEGF-C is transported by extracellular vesicles (EVs) to

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

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

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

145 Our results have identified VEGF-C, YAP and TAZ as a crucial molecular pathway in va

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

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

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

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

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

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

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

153 , via suppression of COUP-TFII level, induce VEGF-C overexpression.

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

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

156 Knockdown of ARRB1 inhibited VEGF-C-induced endothelial cell proliferation, migration

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

158 cells can be disrupted by either inhibiting VEGF-C in EMT cells or by knocking down NRP2, a receptor

159 mass spectrometric analysis of the isolated VEGF-C-cleaving activity from human saliva, we identifie

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

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

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

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

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

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

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

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

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

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

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

171 163(+)/CD68(+)/VEGFC(+) cells and absence of VEGF-C expression by CD3(+) or CD11C(+) cells suggested

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

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

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

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

176 Exogenous administration of VEGF-C via an adenoassociated viral vector improved hema

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

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

179 These results reveal the capacity of VEGF-C to promote immune surveillance of tumours, and su

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

202 the ERK/AKT pathway in HLECs independent of VEGF-C.

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

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

205 Intravitreal OPT-302 inhibition of VEGF-C and -D was well tolerated, and OPT-302 combinatio

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

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

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

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

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

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

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

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

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

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

216 EMT cell-induced production and secretion of VEGF-C.

217 is under the nascent renal pelvis; a site of VEGF-C expression, to form a patent vascular plexus.

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

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

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

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

222 In FXII-HAE, only VEGF-C levels were increased.

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

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

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

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

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

228 us cell carcinoma secrete prolymphangiogenic VEGF-C.

229 However, the mechanisms of PROX1/VEGF-C feedback loop remain poorly understood.

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

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

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

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

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

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

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

237 eceptor (VEGFR) 3-Ig in the skin, scavenging VEGF-C and VEGF-D, the role of lymphangiogenesis in the

238 agonist of lymphangiogenesis by sequestering VEGF-C.

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

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

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

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

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

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

245 d increase miR-185-5p expression to suppress VEGF-C expression, yet this miR-185-5p effect on VEGF-A

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

247 he vicious cycle of inflammation, COUP-TFII, VEGF-C, and lymphangiogenesis in the endometriotic micro

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

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

250 y in human breast cancer, demonstrating that VEGF-C strongly correlates with activation of Hedgehog s

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

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

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

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

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

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

257 ar biological characterization revealed that VEGF-C is negatively regulated by an orphan nuclear rece

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

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

260 We show that VEGF-C, secreted by breast cancer cells that have underg

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

262 Here, we report for the first time that VEGF-C signaling is necessary for valve morphogenesis.

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

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

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

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

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

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

269 PROX1 promotes the expression of the VEGF-C receptor VEGFR3 in lymphatic endothelial cells (L

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

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

272 Our study suggests that the VEGF-C/NRP2/GLI axis is a novel and conserved paracrine

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

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

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

276 X1 expression in LVs and LVVs in response to VEGF-C signaling.

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

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

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

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

281 Evaluation of EV-transmitted VEGF-C from patients' sera demonstrates it is a reliable

282 In turn, VEGF-C signaling maintains PROX1 expression in LECs.

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

284 Here we describe a novel, unique VEGF-C form in the human reproductive system produced vi

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

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

287 the integrity of the perivascular niche via VEGF-C signaling could be exploited therapeutically to e

288 y activated in CLNs within 24 h, in part via VEGF-C/VEGFR3 signalling.

289 In vitro, VEGF-C/VEGFR3 signalling in lymphatic endothelial cells

290 The differential regulation of VEGF-A vs VEGF-C by AR may then result in differential impacts on

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

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

293 Whether VEGF-C signaling is necessary for LV and LVV development

294 tanding functional differences compared with VEGF-C.

295 perm liquefaction occurred concurrently with VEGF-C activation, which was enhanced by collagen and ca

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

297 g down NRP2, a receptor which interacts with VEGF-C, in neighboring epithelial cancer cells.

298 ymphatic vasculature can be manipulated with VEGF-C to promote an immune response to glioblastoma.

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

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