ライフサイエンスコーパス: VEGF-B

1 VEGF-B also prevented capillary rarefaction in the heart

2 VEGF-B also protected cultured endothelial cells from ap

3 VEGF-B and placental growth factor (PlGF) activate VEGFR

4 VEGF-B Blockade with the Monoclonal Antibody CSL346 in S

5 VEGF-B increased left ventricular volume without comprom

6 VEGF-B is closely related to VEGF-A and placenta growth

7 VEGF-B may provide novel therapeutic strategies for the

8 VEGF-B prevented LV wall thinning but did not induce car

9 VEGF-B primarily provides neuroprotection and improves s

10 VEGF-B residues essential for binding to the antibody ar

11 VEGF-B treatment completely inhibited the DOX-induced ca

12 VEGF-B treatment increased nerve regeneration, sensation

13 VEGF-B, a homolog of VEGF discovered a long time ago, ha

14 VEGF-B, angiopoietin-1, angiopoietin-2, and a VEGF/angio

15 VEGF-B-induced neurite elongation required PI3K and Notc

16 IGF-2-, VEGF-B- or VEGF-D-stimulated chondrosarcoma cells displa

17 rdiac endothelium (aP2 [adipocyte protein 2]-VEGF-B) was associated with septal defects and failure t

18 tracing was used to identify the origin of a VEGF-B-induced novel endothelial cell population and ade

19 cept ('VEGF Trap', which neutralizes VEGF-A, VEGF-B and PlGF) showed greater efficacy than nesvacumab

20 the VEGF family, but in contrast to VEGF-A, VEGF-B does not regulate blood vessel growth.

21 er of the VEGFR family, and binds to VEGF-A, VEGF-B, and placental growth factor.

22 ns from native VEGF receptors, binds VEGF-A, VEGF-B, and placental growth factors 1 and 2 with high a

23 t [mFlt(1-3)-IgG], which neutralizes VEGF-A, VEGF-B, and PlGF.

24 d R2), or neutralizing antibodies to VEGF-A, VEGF-B, or fibroblast growth factor (FGF)-2.

25 be involved, but the precise role of VEGF-A, VEGF-B, placental growth factor (PlGF), and their recept

26 The expression of VEGF-A, VEGF-B, PlGF, VEGFR1, and VEGFR2 was measured in NP (n =

27 ated with cervical cancer, including VEGF-A, VEGF-B, VEGF-C, VEGF-D, and VEGF-E, show upregulation an

28 ntricular (LV) end-diastolic pressure in AAV-VEGF-B and AAV-control was, respectively, 15.0+/-1.5 ver

29 of apoptosis, was superphysiological in AAV-VEGF-B, whereas the proapoptotic intracellular mediators

30 ere activated in AAV-control, but not in AAV-VEGF-B.

31 failure, whereas the VEGF-B-transduced (AAV-VEGF-B, n=8) were still in a well-compensated state, wit

32 c VEGF-B transgene (myosin heavy chain alpha-VEGF-B), autocrine VEGF-B expression in cardiac endothel

33 of vascular cells, we revealed that although VEGF-B is dispensable for blood vessel growth, it is cri

34 by 8 hours post-mTBI, particularly GAS-1 and VEGF-B were increased while CXCL16 reduced, 23 proteins

35 Tumor-derived VEGF-A, PLGF-2, and VEGF-B augment pain sensitivity through selective activa

36 e L3.6pl with the VEGFR-1 ligands VEGF-A and VEGF-B led to morphologic changes characteristic of EMT,

37 nclusion, our findings suggest that PlGF and VEGF-B do not compensate during conditions of VEGF-A blo

38 Expression levels of VEGFR1 and VEGF-B correlate with edema and clinical markers of NP d

39 control tissue, without altering VEGFR1 and VEGF-B expression.

40 mRNA expression of VEGFR1 and VEGF-B was significantly higher in NP compared with cont

41 tivity in animal models of DKD using an anti-VEGF-B antibody improved histological evidence of glomer

42 thological angiogenesis, a neutralising anti-VEGF-B antibody (2H10) that functions by inhibiting the

43 The surviving aP2-VEGF-B offspring showed an altered ratio of secreted VEG

44 (myosin heavy chain alpha-VEGF-B), autocrine VEGF-B expression in cardiac endothelium (aP2 [adipocyte

45 However, autocrine VEGF-B signaling fails to promote VEGF-B-induced endothe

46 ls) of endocardial origin, whereas autocrine VEGF-B increased proliferation of VEGF-B-induced endothe

47 reased vascular endothelial growth factor B (VEGF-B) expression in patients with diabetic kidney dise

48 Vascular endothelial growth factor-B (VEGF-B) is a member of the VEGF family of growth factors

49 d that vascular endothelial growth factor-B (VEGF-B), which promotes coronary arteriogenesis, physiol

50 f vascular endothelial growth factor type B (VEGF-B) and VEGF-A, respectively.

51 gest that functional complementarity between VEGF-B and 2H10 can be harnessed both in analysing the t

52 vel humanized monoclonal antibody that binds VEGF-B with high affinity.

53 absence of compensatory VEGFR-1 signaling by VEGF-B and PlGF may have important implications for the

54 AAV-9-carried VEGF-B(167) cDNA (10(12) genome copies) was injected int

55 ficantly correlated with NP albumin content (VEGF-B: P = 0.0208; VEGFR1: P = 0.0293), CT scan scores

56 y inhibiting DOX-induced endothelial damage, VEGF-B could provide a novel therapeutic possibility for

57 This study evaluated VEGF-B gene therapy in a canine model of tachypacing-ind

58 in all paced dogs, suggesting that exogenous VEGF-B(167) exerted a compensatory receptor stimulation.

59 an adeno-associated viral vector expressing VEGF-B or control vector to normal and tumor-bearing mic

60 GF homologues (e.g. placental growth factor, VEGF-B, and VEGF-C), which may play a role in angiogenes

61 of PR39 or another angiogenic growth factor, VEGF-B, into murine hearts during myocardial infarction

62 We revealed here a novel function for VEGF-B as a potent inhibitor of apoptosis.

63 There is growing evidence of a role for VEGF-B in physiological and pathological blood vessel an

64 in VEGFR1 or VEGFR2 concentration with 24 h VEGF-B(167) treatment.

65 ve determined the crystal structure of human VEGF-B(10-108) at 2.48 Angstroms resolution.

66 ytes exposed to 10(-8) mol/L angiotensin II: VEGF-B(167) prevented oxidative stress, loss of mitochon

67 Importantly, VEGF-B did not affect serum or tissue concentrations of

68 mpare cardiac endothelial gene expression in VEGF-B transgenic mouse models.

69 ions of injured corneal peripheral nerves in VEGF-B-deficient and wild-type animals, without affectin

70 Instead, VEGF-B controls endothelial fatty acid (FA) uptake and w

71 Interestingly, VEGF-B treatment at the dose effective for neuronal surv

72 ses VEGFR-1 (Flt-1) and VEGFR-2 (Flk-1/KDR), VEGF-B and PlGF bind to VEGFR-1 and not VEGFR-2.

73 for normal nerve regeneration: mice lacking VEGF-B showed impaired nerve repair with concomitant imp

74 of a novel cardiac endothelial cell lineage (VEGF-B-induced endothelial cells) of endocardial origin,

75 es and its lack of angiogenic activity makes VEGF-B a suitable therapeutic target to treat nerve inju

76 0.0075; VEGFR1: P = 0.0068), and IL-5 mRNA (VEGF-B: P = 0.0027; VEGFR1: P = 0.0001).

77 hway by which VEGF-A and VEGF-E, but neither VEGF-B, nor PlGF, induce the interaction of VEGFR2/KDR w

78 ant, we found that VEGF-A or VEGF-E, but not VEGF-B, nor placenta growth factor (PlGF), induces the p

79 ent a predicted model for the association of VEGF-B with the second domain of its receptor, VEGFR-1.

80 that functions by inhibiting the binding of VEGF-B to VEGF receptor 1 was developed.

81 othesized that the relative contributions of VEGF-B and PlGF to VEGFR-1 signaling may be masked in th

82 e found that the vascular survival effect of VEGF-B is achieved by regulating the expression of many

83 Importantly, the survival effect of VEGF-B is not only on vascular endothelial cells, but al

84 genesis-unrelated cardioprotective effect of VEGF-B(167) in nonischemic dilated cardiomyopathy, which

85 for the beneficial versus adverse effects of VEGF-B in the heart, we explored the cardiac effects of

86 ated gene delivery to compare the effects of VEGF-B isoforms.

87 These selective effects of VEGF-B on injured nerves and its lack of angiogenic acti

88 The cytoprotective effects of VEGF-B(167) were further elucidated in cultured rat neon

89 ighly induced mRNA and protein expression of VEGF-B, which was assumed to be a downstream target of t

90 Our work thus indicates that the function of VEGF-B in the vascular system is to act as a "survival,"

91 family members, the biological functions of VEGF-B remain poorly understood.

92 Expression levels of VEGF-B and VEGFR1 significantly correlated with NP album

93 dies have shown the therapeutic potential of VEGF-B (vascular endothelial growth factor B) in revascu

94 th in analysing the therapeutic potential of VEGF-B and as an antagonist of receptor activation.

95 y the specifics of the biological profile of VEGF-B in both physiological and pathological angiogenes

96 autocrine VEGF-B increased proliferation of VEGF-B-induced endothelial cells but failed to promote t

97 Paracrine and autocrine secretions of VEGF-B induce expansion of a specific endocardium-derive

98 VEGF-A (a ligand for both VEGFR-1 and -2) or VEGF-B (a ligand specific for VEGFR-1) led to activation

99 We report here that VEGF-A or VEGF-B induces VEGFR-1-mediated ERK1/2 phosphorylation i

100 GFR-2 and NRP1 are not needed for VEGF-A- or VEGF-B-induced ERK1/2 activation.

101 Paracrine VEGF-B led to robust proliferation and myocardial migrat

102 ardiac effects of autocrine versus paracrine VEGF-B expression in transgenic and gene-transduced mice

103 autocrine VEGF-B signaling fails to promote VEGF-B-induced endothelial cell migration and contributi

104 ve effect was obtained using the recombinant VEGF-B, suggesting the involvement of VEGF-R1 pathway in

105 Reducing VEGF-B activity in animal models of DKD using an anti-VE

106 0.0208; VEGFR1: P = 0.0293), CT scan scores (VEGF-B: P = 0.0075; VEGFR1: P = 0.0068), and IL-5 mRNA (

107 ffspring showed an altered ratio of secreted VEGF-B isoforms and developed massive pathological cardi

108 In the normal heart, we found a small VEGF-B-induced endothelial cell population that was only

109 pertrophy driven by a cardiomyocyte-specific VEGF-B transgene (myosin heavy chain alpha-VEGF-B), auto

110 Targeting VEGF-B in patients with type 2 diabetes mellitus may imp

111 rather than an "angiogenic" factor and that VEGF-B inhibition may offer new therapeutic opportunitie

112 We found that VEGF-B induced extensive neurite growth and branching in

113 These findings indicate that VEGF-B may potentially offer a new therapeutic option fo

114 An important recent discovery is that VEGF-B produced by skeletal muscle controls the expressi

115 We observe that VEGF-B(167) induces little to no change in either VEGFR1

116 ing mouse and rat cell lines, we showed that VEGF-B inhibited the expression of genes encoding the pr

117 We suggest that VEGF-B is the missing link between PGC-1alpha overexpres

118 retinal neovascularization, suggesting that VEGF-B is the first member of the VEGF family that has a

119 al binding sites located at each pole of the VEGF-B homodimer, giving a unique U-shaped topology to t

120 overt congestive heart failure, whereas the VEGF-B-transduced (AAV-VEGF-B, n=8) were still in a well

121 Therefore, VEGF-B might be an ideal candidate for the treatment of

122 Consistent with this, VEGF-B treatment rescued neurons from apoptosis in the r

123 Antibodies to VEGF-B, but not VEGF-A, had a strong inhibitory effect o

124 The levels of bFGF and VEGF (VEGF, VEGF-B, and VEGF-C) in corneal epithelial cells were not

125 In vivo, VEGF-B is required for normal nerve regeneration: mice l

126 In vivo, VEGF-B targeting inhibited both choroidal and retinal ne

127 We examined whether VEGF-B mediates peripheral nerve repair.

128 ab fragment of this antibody (Fab-2H10) with VEGF-B.