Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.26.9 (ribonuclease)
 6,589 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vascular endothelial growth factor (VEGF) functions as a potent angiogenic protein as well as in regulating permeability. Reverse transcription-polymerase chain reaction (RT-PCR) and ribonuclease protection assay (RPA) were used to show that the bovine oviduct expresses VEGF and its two receptors flk-1 and flt-1. Expression of VEGF was relatively stable during the estrous cycle. In contrast, both receptor transcripts showed cycle-dependent variations with significantly increased flt-1 mRNA amounts before ovulation. Immunohistochemical studies localized VEGF mainly on the epithelial surface of oviducts. Protein concentrations of VEGF in oviductal flushings were significantly higher (mean +/- SEM: 2.8 +/- 0.8 ng/ml) during the pre-ovulatory phase when compared with the other estrous cycle stages (1.0 +/- 0.25 ng/ml). In conclusion, all components of a functional VEGF-system in the bovine oviduct were found to undergo specific modulations during the cycle. We suggest that VEGF may be involved in creating an optimal local environment for fertilization or the developing embryo by modulating permeability within the bovine oviduct.
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PMID:Expression of vascular endothelial growth factor (VEGF) and its corresponding receptors (flt-1 and flk-1) in the bovine oviduct. 1039 12

Angiogenesis is essential for tumour growth and metastasis. It is regulated by numerous angiogenic factors, one of the most important being vascular endothelial growth factor (VEGF). Recently VEGF-B, a new VEGF family member that binds to the tyrosine kinase receptor flt-1, has been identified. Although the importance of VEGF has been shown in many human tumour types, the contribution of VEGF-B to tumour neovascularization is unknown in any tumour type. 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. Flt-1 expression was significantly higher in tumours than in normal breast (p=0.02) but no significant difference was seen in VEGF-B between normal and neoplastic breast (p=0.3). There was a significant association between VEGF-B and node status (p=0.02) and the number of involved nodes (p=0.01), but not with age (p=0.7), size (p=0.6), oestrogen receptor (ER) (p=0.2), grade (p=0.5) or vascular invasion (p=0.16). No significant relationship was present between VEGF-B and flt-1 (p=0.2) or tumour vascularity (p=0.4). VEGF-B was expressed mostly in the cytoplasm of tumour cells, although occasional stromal components including fibroblasts and endothelial cells were also positive. No difference in VEGF-B expression was observed adjacent to regions of necrosis, in keeping with this VEGF family member not being hypoxically regulated. These findings suggest that VEGF-B may contribute to tumour progression by a non-angiogenic mechanism, possibly by increasing plasminogen activators and hence metastasis, as has been described in vitro. Measurement of VEGF-B together with other angiogenic factors may identify a poor prognostic patient group, which may benefit from anti-VEGF receptor therapy targeted to flt-1 (VEGFR1) as well as kdr (VEGFR2).
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PMID:VEGF-B expression in human primary breast cancers is associated with lymph node metastasis but not angiogenesis. 1124 11