Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027960 (mole)
21,279 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The chick chorioallantoic membrane assay was employed to assess the angiogenic response induced by mixtures of human angiogenin with bovine heparin-binding acidic fibroblast growth factor. Statistical evaluation of data accumulated at several molar ratios of the two proteins indicate that the angiogenic activity observed is neither an additive nor a synergistic resultant of the activities of the proteins separately. The possibility exists, however, that at an approximately 1:1 mole ratio an apparent inhibitory effect can be observed. Mechanisms which could underlie such observed effects are discussed.
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PMID:Induction of angiogenesis by mixtures of two angiogenic proteins, angiogenin and acidic fibroblast growth factor, in the chick chorioallantoic membrane. 244 1

Angiogenin is a potent inducer of blood-vessel formation with ribonucleolytic activity. Angiogenin binds to high affinity endothelial cell receptors and with lower affinity to extracellular matrix components. Here we report the effect of copper and zinc on these interactions. There was a 4.3-fold increase in angiogenin binding to calf pulmonary artery endothelial cells in the presence of Cu2+ in vitro. A 3.8-fold increase was observed with Zn2+, whereas Ni2+, Co2+, or Li+ had no effect. Specific angiogenin binding to the lower affinity matrix sites was increased by 2.7- and 1.9-fold in the presence of Cu2+ and Zn2+ respectively. Metal ion affinity chromatography and atomic absorption spectrometry were used to show the direct interaction of angiogenin with copper and zinc ions. Angiogenin bound 2.4 mol of copper per mole of protein. We suggest that copper, a modulator of angiogenesis in vivo, may be involved in the regulation of the biological activity of angiogenin.
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PMID:Interaction of human angiogenin with copper modulates angiogenin binding to endothelial cells. 924 97

Angiogenesis is essential for tumor progression and metastasis, however, the angiogenesis regulators that are biologically relevant for human melanoma are still unknown. In this study, we analyzed the expression of the potent angiogenic factor angiogenin (ANG) in human melanoma in vitro and in vivo. Four different human melanoma cell lines and two normal melanocytes were kept either under normoxic or hypoxic conditions. After 24 h of hypoxic culture conditions, ANG was up-regulated in the melanoma cell lines but not in normal melanocytes. Induction levels correlated with the metastatic potential of the cell lines. These data were confirmed by Northern blot analysis. In contrast, induction of vascular endothelial growth factor by hypoxia was equally strong in the examined highly aggressive melanoma cell lines and in one nonaggressive cell line. Other angiogenic factors tested as well as the melanoma growth stimulatory activity (Gro-alpha) showed no up-regulation. Thus, in the present study, hypoxia-induced up-regulation in melanoma cells was only observed for ANG and vascular endothelial growth factor. Immunohistochemical studies showed that 8 of 10 melanomas and all 15 metastases were positive for ANG, particularly in the vicinity of small vessels, whereas all benign nevi were negative. Reverse transcription-PCR detected only weak ANG mRNA in nevi but strong signals in primary melanomas and metastases. In conclusion, we demonstrate for the first time enhanced expression of ANG in highly metastatic cell lines as well as in melanomas and metastases in vivo, suggesting that ANG expression is associated with the metastatic potential.
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PMID:Hypoxia-induced up-regulation of angiogenin in human malignant melanoma. 1019 32

The aim of this study was to evaluate the diagnostic and prognostic values of serum angiogenin concentration in cases with gestational trophoblastic diseases (GTDs). Seventy-two patients with GTDs and 20 first trimester healthy pregnant women (controls) participated in this study. According to the WHO scoring system, GTDs were subgrouped into 24 hydatiform mole spontaneous regression (HMSR), 18 postmolar gestational trophoblastic tumors of high risk (PMHR), 16 low-risk choriocarcinoma, and 14 high-risk choriocarcinoma. Before treatment, a blood sample from each case was assayed for human chorionic gonadotrophin , subunit (hCGb) by radioimmunoassay and angiogenin by enzyme immunoassay. Follow-up hCGb and angiogenin assays were carried out for 1 year after treatment. Pretreatment of abnormal values of serum angiogenin (> 711 ng/ml, upper 95% confidence interval of controls) was encountered in 100% of PMHR cases compared to no single case of HMSR. Serum angiogenin levels in low- and high-risk cases with choriocarcinoma were significantly higher than in controls. Abnormal high values were encountered in 25% and 86% of cases, respectively. None of the low-risk cases exceeded 920 ng/ml, while 72% of high-risk cases exceeded this value. Serial angiogenin assays were correlated with disease progression and were positively correlated with serum hCGb (r = 0.75, p < 0.01). In conclusion, serum angiogenin may be a valuable marker of differential diagnosis of GTDs and its serial measurements are suggestive of remission and effective therapeutic intervention or disease progression.
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PMID:Angiogenin and gestational trophoblastic tumors, a promising prognostic marker. 1270 39