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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 increased left ventricular volume without comprom
5 VEGF-B is closely related to VEGF-A and placenta growth
6 VEGF-B may provide novel therapeutic strategies for the
7 VEGF-B prevented LV wall thinning but did not induce car
8 VEGF-B primarily provides neuroprotection and improves s
9 VEGF-B residues essential for binding to the antibody ar
10 VEGF-B treatment completely inhibited the DOX-induced ca
11 VEGF-B treatment increased nerve regeneration, sensation
12 VEGF-B, a homolog of VEGF discovered a long time ago, ha
13 VEGF-B, angiopoietin-1, angiopoietin-2, and a VEGF/angio
14 VEGF-B-induced neurite elongation required PI3K and Notc
16 cept ('VEGF Trap', which neutralizes VEGF-A, VEGF-B and PlGF) showed greater efficacy than nesvacumab
19 ns from native VEGF receptors, binds VEGF-A, VEGF-B, and placental growth factors 1 and 2 with high a
22 be involved, but the precise role of VEGF-A, VEGF-B, placental growth factor (PlGF), and their recept
24 ntricular (LV) end-diastolic pressure in AAV-VEGF-B and AAV-control was, respectively, 15.0+/-1.5 ver
25 of apoptosis, was superphysiological in AAV-VEGF-B, whereas the proapoptotic intracellular mediators
27 failure, whereas the VEGF-B-transduced (AAV-VEGF-B, n=8) were still in a well-compensated state, wit
28 of vascular cells, we revealed that although VEGF-B is dispensable for blood vessel growth, it is cri
30 e L3.6pl with the VEGFR-1 ligands VEGF-A and VEGF-B led to morphologic changes characteristic of EMT,
31 nclusion, our findings suggest that PlGF and VEGF-B do not compensate during conditions of VEGF-A blo
35 thological angiogenesis, a neutralising anti-VEGF-B antibody (2H10) that functions by inhibiting the
37 d that vascular endothelial growth factor-B (VEGF-B), which promotes coronary arteriogenesis, physiol
39 gest that functional complementarity between VEGF-B and 2H10 can be harnessed both in analysing the t
40 absence of compensatory VEGFR-1 signaling by VEGF-B and PlGF may have important implications for the
42 ficantly correlated with NP albumin content (VEGF-B: P = 0.0208; VEGFR1: P = 0.0293), CT scan scores
43 y inhibiting DOX-induced endothelial damage, VEGF-B could provide a novel therapeutic possibility for
45 in all paced dogs, suggesting that exogenous VEGF-B(167) exerted a compensatory receptor stimulation.
46 an adeno-associated viral vector expressing VEGF-B or control vector to normal and tumor-bearing mic
47 GF homologues (e.g. placental growth factor, VEGF-B, and VEGF-C), which may play a role in angiogenes
48 of PR39 or another angiogenic growth factor, VEGF-B, into murine hearts during myocardial infarction
52 ytes exposed to 10(-8) mol/L angiotensin II: VEGF-B(167) prevented oxidative stress, loss of mitochon
54 ions of injured corneal peripheral nerves in VEGF-B-deficient and wild-type animals, without affectin
58 for normal nerve regeneration: mice lacking VEGF-B showed impaired nerve repair with concomitant imp
59 es and its lack of angiogenic activity makes VEGF-B a suitable therapeutic target to treat nerve inju
61 hway by which VEGF-A and VEGF-E, but neither VEGF-B, nor PlGF, induce the interaction of VEGFR2/KDR w
62 ant, we found that VEGF-A or VEGF-E, but not VEGF-B, nor placenta growth factor (PlGF), induces the p
63 ent a predicted model for the association of VEGF-B with the second domain of its receptor, VEGFR-1.
65 othesized that the relative contributions of VEGF-B and PlGF to VEGFR-1 signaling may be masked in th
66 e found that the vascular survival effect of VEGF-B is achieved by regulating the expression of many
68 genesis-unrelated cardioprotective effect of VEGF-B(167) in nonischemic dilated cardiomyopathy, which
71 ighly induced mRNA and protein expression of VEGF-B, which was assumed to be a downstream target of t
72 Our work thus indicates that the function of VEGF-B in the vascular system is to act as a "survival,"
76 y the specifics of the biological profile of VEGF-B in both physiological and pathological angiogenes
77 VEGF-A (a ligand for both VEGFR-1 and -2) or VEGF-B (a ligand specific for VEGFR-1) led to activation
80 0.0208; VEGFR1: P = 0.0293), CT scan scores (VEGF-B: P = 0.0075; VEGFR1: P = 0.0068), and IL-5 mRNA (
81 rather than an "angiogenic" factor and that VEGF-B inhibition may offer new therapeutic opportunitie
85 ing mouse and rat cell lines, we showed that VEGF-B inhibited the expression of genes encoding the pr
87 retinal neovascularization, suggesting that VEGF-B is the first member of the VEGF family that has a
88 al binding sites located at each pole of the VEGF-B homodimer, giving a unique U-shaped topology to t
89 overt congestive heart failure, whereas the VEGF-B-transduced (AAV-VEGF-B, n=8) were still in a well
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