ライフサイエンスコーパス: VEGF-D

1 VEGF-D activated extracellular signal-regulated protein

2 VEGF-D failed to induce cell migration in the absence of

3 VEGF-D induced KDR and phospholipase C-gamma tyrosine ph

4 VEGF-D induced strong but more transient phosphatidylino

5 VEGF-D is an angiogenic and lymphangiogenic glycoprotein

6 VEGF-D stimulated chemotaxis via a PI3K/Akt- and endothe

7 VEGF-D-induced signaling and biological effects were blo

8 In contrast to VEGF-A, VEGF-D weakly stimulated prostacyclin production and gen

9 elta N Delta C encoded by the adenovirus (Ad-VEGF-D Delta N Delta C) is capable of inducing endotheli

10 trated that neovascularization induced by Ad-VEGF-D Delta N Delta C and by Ad-VEGF-A(165) (an adenovi

11 In a skin model, Ad-VEGF-D Delta N Delta C induced angiogenesis and lymphang

12 The capacity of Ad-VEGF-D Delta N Delta C to induce endothelial cell prolif

13 In this model, a proangiogenic effect of Ad-VEGF-D Delta N Delta C was evident as early as 5 days af

14 Adipose VEGF-D overexpression induced de novo lymphangiogenesis

15 into the preservation solution alone (alpha-VEGF D/-), in the preservation solution and systemically

16 was only reduced in alpha-VEGF D/R and alpha-VEGF D/- groups versus Perfadex controls.

17 VEGF-A blockade in alpha-VEGF D/-, alpha-VEGF D/R, and alpha-VEGF -/R resulted in neutralization

18 VEGF-A blockade in alpha-VEGF D/-, alpha-VEGF D/R, and alpha-VEGF -/R resulted in

19 Reperfusion edema was only reduced in alpha-VEGF D/R and alpha-VEGF D/- groups versus Perfadex contr

20 y to the recipient before reperfusion (alpha-VEGF D/R), or applied to the recipient alone before repe

21 Whereas generally the alpha-VEGF D/- group showed decreased inflammation, the combin

22 at differential KDR activation by VEGF-A and VEGF-D has distinct consequences for endothelial signali

23 cular endothelial growth factor (VEGF)-A and VEGF-D.

24 on-dependent fashion showing that VEGF-C and VEGF-D are ligands for the integrin alpha9beta1.

25 VEGF-C and VEGF-D are secreted glycoproteins that induce angiogenes

26 cular endothelial growth factor (VEGF)-C and VEGF-D by adeno-associated viral vector-mediated soluble

27 ptor VEGFR3 or global loss of the VEGF-C and VEGF-D ligands.

28 e, we have studied the effects of VEGF-C and VEGF-D on tumor development in the murine multistep chem

29 VEGF-C and VEGF-D were identified as lymphangiogenic growth factors

30 cular endothelial growth factor (VEGF)-C and VEGF-D were identified.

31 VEGF-C and VEGF-D were thought to exhibit similar bioactivities, ye

32 lymphangiogenic stimuli including VEGF-C and VEGF-D with temporally regulated expression levels durin

33 GFR) 3-Ig in the skin, scavenging VEGF-C and VEGF-D, the role of lymphangiogenesis in the generation

34 elium to VEGFR-3 binding factors, VEGF-C and VEGF-D, ultimately resulting in robust lymphangiogenesis

35 cular endothelial growth factor (VEGF)-C and VEGF-D.

36 s of the VPF/VEGF family, namely, VEGF-C and VEGF-D.

37 nse to the binding of the ligands VEGF-C and VEGF-D.

38 that is activated by its ligands VEGF-C and VEGF-D.

39 lar endothelial growth factor C (VEGF-C) and VEGF-D have been described as key players in BCa-induced

40 VEGF signaling molecules VEGF-A, VEGF-C, and VEGF-D.

41 d expression of VEGFR-2, VEGF-A, VEGF-C, and VEGF-D.

42 inhibited cell migration induced by ECM and VEGF-D, indicating that signals from both beta(1) integr

43 In the case of FR and VEGF-D, in which incorporation is confined to upstream r

44 opn-2, VEGF-A, IP-10, PDGF, KGF, angiogenin, VEGF-D, ICAM-1, and FGF in plasma samples from 40 patien

45 protease that can activate VEGF-C as well as VEGF-D.

46 Augmenting VEGF-D signaling and lymphangiogenesis specifically in a

47 pathways and biological responses induced by VEGF-D and VEGF-A in endothelial cells.

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

49 HV-8) express higher levels of VEGF, VEGF-C, VEGF-D, and PlGF in addition to VEGF receptors-1, -2, an

50 al cancer, including VEGF-A, VEGF-B, VEGF-C, VEGF-D, and VEGF-E, show upregulation and are linked to

51 luble TIE-1, soluble VEGFR1, VEGF-A, VEGF-C, VEGF-D, VEGF-A isoform 121, bone morphogenetic protein 7

52 These findings indicate that VEGF-C/VEGF-D are involved in shaping the inflammatory tumor mi

53 ous cell carcinoma by using a soluble VEGF-C/VEGF-D inhibitor.

54 transgenic mice expressing a soluble VEGF-C/VEGF-D receptor (sVEGFR-3) in the skin developed signifi

55 lamed corneas release lymphangiogenic VEGF-C/VEGF-D, we evaluated the possibility that macrophage rec

56 Our results support the use of VEGF-C/VEGF-D-blocking agents not only to inhibit metastatic pr

57 In human tumor cells, VEGF-D colocalized with eIF4GI and 4E-BP1, which can pro

58 serum vascular endothelial growth factor D (VEGF-D), and quality of life and functional performance.

59 Vascular endothelial growth factor D (VEGF-D), well-characterized as a "lymphangiogenic" growt

60 (PSA), vascular endothelial growth factor-D (VEGF-D), ETS-related gene protein (ERG), and insulin-lik

61 vascular endothelial growth factor (VEGF)-D, VEGF-D Delta N Delta C, to induce angiogenesis, lymphang

62 (c-fos-induced growth factor) gene encoding VEGF-D have not been reported previously.

63 levels of the lymphangiogenic growth factor VEGF-D are elevated significantly in lymphangioleiomyoma

64 The vascular endothelial growth factor VEGF-D promotes metastasis by inducing lymphangiogenesis

65 Here we report a novel level of control for VEGF-D expression at the level of protein translation.

66 and lymphatics expressing the receptors for VEGF-D in a given tissue.

67 N- or C-terminal propeptide is required for VEGF-D to drive formation of VEGFR-2/VEGFR-3 heterodimer

68 l correlate, and support a critical role for VEGF-D in lung vascular development and homeostasis.

69 We compared the percent change in VEGF-D levels (baseline to 24 months) in patients from t

70 (removal of this propeptide from full-length VEGF-D completely prevents heparin binding).

71 y the C-terminal propeptide from full-length VEGF-D was sufficient to enhance angiogenesis and tumor

72 anced when a gradient of the cognate ligand, VEGF-D, was added.

73 te that the N-terminal alpha-helix of mature VEGF-D (Phe(93)-Arg(108)) is critical for binding VEGFR-

74 A variant of mature VEGF-D harboring a mutation in the N-terminal alpha-heli

75 The lymphangiogenic molecules VEGF-D and angiopoietin-2 were elevated in the plasma of

76 At 24 months, VEGF-D levels decreased by 67% compared with baseline (t

77 c ligands (VEGF-C156S and recombinant murine VEGF-D) into the corneal stroma induce not only LA but a

78 e we investigated the mechanism of action of VEGF-D, and we compared the signaling pathways and biolo

79 e the basis of the distinct bioactivities of VEGF-D using a neutralizing antibody, peptide mapping, a

80 se data suggest that the biologic effects of VEGF-D are tissue-specific and dependent on the abundanc

81 neural crest and SMC markers, expression of VEGF-D and female sex hormone receptors, reduced autopha

82 oedema and we find widespread expression of VEGF-D, rigf and Ang2a in the talpid(3) limb.

83 The mature form of VEGF-D, lacking both propeptides, can also promote forma

84 will be important to clarify which forms of VEGF-D are biologically active and therefore clinically

85 ofoundly influence molecular interactions of VEGF-D with VEGF receptors, co-receptors, and heparin, a

86 In murine tumors, the steady-state level of VEGF-D protein was increased despite the overexpression

87 Furthermore, levels of VEGF-D and MCP-1 in patient sera correlated positively w

88 ar cells (PBMC) stimulated the production of VEGF-D.

89 lts identify nucleolin as a key regulator of VEGF-D expression, deepening understanding of lymphangio

90 l maturation, bound directly to the 5'UTR of VEGF-D mRNA, thereby improving its translation following

91 ribosome entry site (IRES) in the 5' UTR of VEGF-D mRNA.

92 riven by myoepithelial-derived VEGF-C and/or VEGF-D.

93 IGF-2-, VEGF-B- or VEGF-D-stimulated chondrosarcoma cells display markedly

94 Adenoviral delivery of either VEGF-C or VEGF-D evoked lymphangiogenesis without angiogenesis, wh

95 ation in vitro was not affected by VEGF-C or VEGF-D, indicating indirect effects of sVEGFR-3 expressi

96 ells expressed the VEGFR-3 ligands VEGF-C or VEGF-D.

97 BMCs from lymphangioleiomyomatosis patients, VEGF-D expression was elevated.

98 monitoring of TSC kidney disease, we present VEGF-D level results with 24 month follow-up.

99 g increased expression of prolymphangiogenic VEGF-D and proliferation of lymphatic endothelial cells.

100 ilencing or pharmacologic inhibition reduced VEGF-D translation along with a subsequent constriction

101 wever, there are gaps in knowledge regarding VEGF-D dysregulation and its cellular origin in lymphang

102 oactivity and, to a lesser extent, secreting VEGF-D.

103 Serum VEGF-D was measured in samples collected from subjects e

104 Conclusions Serum VEGF-D may be useful for monitoring response to treatmen

105 To further investigate the utility of serum VEGF-D for longer term monitoring of TSC kidney disease,

106 imus stabilized lung function, reduced serum VEGF-D levels, and was associated with a reduction in sy

107 We have previously shown that serum VEGF-D is elevated at baseline, correlates with kidney a

108 ouse, a model of inducible, adipose-specific VEGF-D overexpression.

109 We report for the first time that VEGF-D binds heparin, and that the C-terminal propeptide

110 We first demonstrated in vitro that VEGF-D Delta N Delta C encoded by the adenovirus (Ad-VEG

111 f valine to methionine at residue 118 of the VEGF-D protein.

112 Our studies shed light on the VEGF-D structure/function relationship and provide a bas

113 Here we use VEGF-D mutants deficient in either propeptide, and in th

114 ere essential for their development, whereas VEGF-D deletion had no effect.

115 tasis via the lymphatic vasculature, whereas VEGF-D did not).