Disease relevance of VEGFB

• Expressions of VEGFB mRNA were affected neither by hypoxia nor by dexamethasone [1].
• The results indicate a coexpression of VEGF mRNA and VEGFB mRNA in human astrocytomas [1].
• Vascular endothelial growth factor-B and vascular endothelial growth factor-C expression in renal cell carcinomas: regulation by the von Hippel-Lindau gene and hypoxia [2].
• VEGF-B may provide novel therapeutic strategies for the treatment of vascular disease and be a potential therapeutic target in aberrant vessel formation [3].
• RESULTS: Treatment with 100 ng/ml progesterone increased VEGF-A, VEGF-B and ADM contents in cultured leiomyoma cells and normal myometrial cells [4].

Psychiatry related information on VEGFB

• We evaluated the efficacy and safety of the centrally acting cholinesterase inhibitor, rivastigmine tartrate, for patients with mild to moderately severe Alzheimer's disease (AD) with or without concurrent vascular risk factors (VRF) [5].

High impact information on VEGFB

• CONCLUSIONS: The VEGF-B locus in 11q13 and the VEGF-C locus in 4q34 are candidate targets for mutations that lead to vascular malformations or cardiovascular diseases [6].
• The VEGF-B gene was found on chromosome 11q13, proximal to the cyclin D1 gene, which is amplified in a number of human carcinomas [6].
• METHODS AND RESULTS: Southern blotting and polymerase chain reaction analysis of somatic cell hybrids and fluorescence in situ hybridization (FISH) of metaphase chromosomes were used to assess the chromosomal localization of VEGF-B and VEGF-C genes [6].
• Our treatment of the human pancreatic cancer cell line L3.6pl with the VEGFR-1 ligands VEGF-A and VEGF-B led to morphologic changes characteristic of EMT, including loss of polarity, increased intercellular separation, and the presence of pseudopodia [7].
• There was also a significant correlation between VEGF-C and both of its receptors flt-4 (P = 0.006) and KDR (P = 0.03) but no association between VEGF-B and its receptor flt-1 (P = 0.23) [2].

Biological context of VEGFB

• A new splice variant of VEGFB (VEGFB155) that lacks exons 5 and 6 is described [1].
• We observed a significant up-regulation of VEGF-B (P = 0.002) but not VEGF-C (P = 0.3) in neoplastic kidney compared with normal tissues [2].
• VEGF and VEGF-B gene expression was quantified by Northern blot in 72 tumor samples matched with control tissues [8].
• Exons 6 and 7 are contiguous and the two isoforms of VRF arise through alternate splicing of exon 6 [9].
• The VRF gene maps to the D11S750 locus at chromosome band 11q13, and the protein coding region, spanning approximately 5 kb, is comprised of 8 exons that range in size from 36 to 431 bp [9].

Anatomical context of VEGFB

• There is growing evidence of a role for VEGF-B in physiological and pathological blood vessel angiogenesis [3].
• VEGF-B mRNA levels were unchanged during the neoplastic progression of colonic mucosa [8].
• Reverse-transcription polymerase chain reaction (RT-PCR) analysis on cultured normal human keratinocytes (NHKs) and normal human fibroblasts (NHFs) allowed the detection of different levels of VEGF-B, -C and -D mRNA, in both cell types with similar RT-PCR products in the skin cells [10].
• The vascular endothelial growth factor (VEGF) family includes the related polypeptides VEGF-B, -C and -D, which contribute to endothelial and lymphatic vessel development [10].
• RESULTS: Saphenous veins showed no staining for VEGF-B or VEGFR-2 [11].

Associations of VEGFB with chemical compounds

• Recently VEGF-B, a new VEGF family member that binds to the tyrosine kinase receptor flt-1, has been identified [12].
• The VEGF-related factor, placenta growth factor (PIGF), had little effect on PGI2 synthesis, arachidonic acid release or cPLA2 activation [13].
• Rivastigmine is effective in both categories of patients, and those with VRF experience greater clinical benefit (cognition, activities of daily living, and disease severity) [5].
• In Condition A, the participant was given a virtual stress assessment scenario relative to a first-person perspective (VRFP) [14].

Physical interactions of VEGFB

• The NRP1 binding of VEGF-B could be competed by an excess of VEGF(165) [15].

Regulatory relationships of VEGFB

• Two representative cell lines (L3.6 and Panc-1) exhibited VEGF-B-induced mitogen-activated protein kinase signaling [16].
• BDNF stimulated mRNA expression of vascular endothelial growth factor-B and tenascin-X, and proliferation and angiogenesis in human endothelial cells [17].

Other interactions of VEGFB

• Vascular endothelial growth factor-B (VEGF-B) is a member of the VEGF family of growth factors that regulate blood vessel and lymphatic angiogenesis [3].
• We also present a predicted model for the association of VEGF-B with the second domain of its receptor, VEGFR-1 [3].
• In contrast VEGF-B was not regulated by VHL despite clear up-regulation in vivo [2].
• The aim of our study was to determine whether the two main skin cells, keratinocytes and fibroblasts, expressed VEGF-B, -C and -D in basal condition and after stimulation by either growth factors or the pro-inflammatory cytokine tumour necrosis factor-alpha (TNF-alpha) [10].
• Three related endothelial cell growth factors, VEGF-B, VEGF-C, and VEGF-D were recently cloned [18].

Analytical, diagnostic and therapeutic context of VEGFB

• Western blotting showed variations in VEGF protein localisation, with lower amounts of VEGF-B and VEGF-C in saphenous veins, compared with arterial tissue [11].
• This study therefore measured the mRNA level of VEGF-B and its receptor flt-1 by ribonuclease protection assay and the pattern of VEGF-B expression by immunohistochemistry in 13 normal breast samples and 68 invasive breast cancers [12].
• We have then utilized RNase protection and ELISA to measure the relative levels of VEGF B, C, D and flt-1, KDR, flt-4 and flt-4t(Delta773-1081) expression in freshly isolated benign prostatic hyperplasia or BPH tissue (n=21), primary prostate cancers (n=82) and matching sentinel lymph node metastases from stage T2a-T2b/T3 tumors (n=52) [19].
• Here, we shall determine if serum levels of vascular endothelial growth factors B and C (VEGF-B, VEGF-C) associated with vasculogenic and lymphogenic metastasis may be used for an early diagnosis of advanced metastatic cervical cancer and compare these levels with those of the serum IGF-II and IGF-binding protein 3 (IGF-BP3) [20].
• The PCR products of VEGF-B (357bp), VEGF-C (501bp), and VEGF-D (484bp) were amplified in all glioblastoma cells examined [21].

References