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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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