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- W2079590804 abstract "To the Editor: Homocysteine has an inhibitory effect on angiogenesis1. However, the vascular endothelial growth factor receptor-2 (VEGFR-2) gene has recently been found up-regulated on human atherosclerotic plaques2. In order to analyze the association between homocysteine and VEGFR-2 serum levels, we have randomly selected 26 regular hemodialysis (HD) patients ages 56 12 years (mean SD; M = 14, F = 12), and 26 age-matched kidney transplanted individuals (KTx), ages 52 8 years (M = 21, F = 5). KTx transplant age was 13 9 months and creatinine was 1.6 0.5 mg/dL. Nine age-matched healthy volunteers (47 5 years) were also recruited. HD samples were collected at the end of the long interval period. Serum homocysteine (Hcy) and VEGFR-2 were tested by high-performance liquid chromatography (HPLC) with fluorimetric detection and a commercial enzyme-linked immunosorbent assay (ELISA) kit, respectively. Hcy was higher in HD patients (57 36 mol/L) than in KTx patients (23 8 mol/L; P < 0.001) and control patients (15 6 mol/L; P < 0.01 vs. HD; P < 0.05 vs. KTx). VEGFR-2 was lower in HD patients (1705 387 pg/mL) than in KTx patients (2449 825 pg/mL; P = 0.014) or control patients (2150 464 pg/mL) Figure 1. The present study shows that Hcy and circulating VEGFR-2 are inversely associated, consistent with previous reports showing that homocysteine inhibits angiogenesis. Our data also suggest that up-regulation of the VEGFR-2 gene is probably a local finding, and that hyperhomocysteinemia may be involved in the release of VEGFR-2 into the systemic circulation." @default.
- W2079590804 created "2016-06-24" @default.
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- W2079590804 date "2003-11-01" @default.
- W2079590804 modified "2023-09-27" @default.
- W2079590804 title "Inverse association between homocysteine and vascular endothelial growth factor receptor 2 serum levels in hemodialyzed and kidney transplanted patients" @default.
- W2079590804 cites W1967511208 @default.
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- W2079590804 doi "https://doi.org/10.1046/j.1523-1755.2003.t01-1-00296.x" @default.
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