Vascular endothelial growth factor (VEGF) promotes neovascularization, microvascular permeability, and endothelial proliferation. We described previously VEGF mRNA and protein induction by estradiol (E2) in human endometrial fibroblasts. We report here E2 induction of VEGF expression in human venous muscle cells [smooth muscle cells (SMC) from human saphenous veins; HSVSMC] expressing both ER-alpha and ER-beta estrogen receptors. E2 at 10(-9) to 10(-8) M increases VEGF mRNA in HSVSMC in a time-dependent manner (3-fold at 24 h), as analyzed by semiquantitative RT-PCR. This level of induction is comparable with E2 endometrial induction of VEGF mRNA. Tamoxifen and hypoxia also increase HSVSMC VEGF mRNA expression over control values. Immunocytochemistry of saphenous veins and isolated SMC confirms translation of VEGF mRNA into protein. Immunoblot analysis of HSVSMC-conditioned medium detects three bands of 18, 23, and 28 kDa, corresponding to VEGF isoforms of 121, 165, and 189 amino acids. Radioreceptor assay of the conditioned medium produced by E2-stimulated HSVSMC reveals an increased VEGF secretion. Our data indicate that VEGF is E2, tamoxifen, and hypoxia inducible in cultured HSVSMC and E2 inducible in aortic SMC, suggesting E2 modulation of VEGF effects in angiogenesis, vascular permeability, and integrity.
Background and Aim: Aflatoxins are metabolites of molds that exert potentially toxic effect on animals and humans. This study aimed to investigate the occurrence of aflatoxin M1 (AFM1) in raw cow milk collected during 1 year (2016-2017) from different regions of Algeria and risk factors associated with the contamination.
Materials and Methods: During the survey period, 84 samples of raw milk were collected in three regions of Algeria (northeast, north center, and northwest) during four seasons. AFM1 levels were analyzed by competitive enzyme-linked immunosorbent assay.
Results: AFM1 was detected in 39 (46.43%) samples (total mean concentration, 71.92 ng/L; range, 95.59-557.22 ng/L). However, the AFM1 levels exceeded the maximum tolerance limit set by the Food and Drug Administration in the USA (500 ng/L) in only 1 sample (1.19%). Statistical analysis revealed significant differences (p<0.005) between AFM1 levels in milk samples collected in the spring and autumn. The mean AFM1 levels in samples collected in the spring were significantly higher than those in samples collected in autumn.
Conclusion: The survey indicates that farmers involved in milk production should be made aware of the adverse effects of aflatoxin contamination in animal feed. A systematic control program of supplementary feedstuff for lactating cows should be introduced by the public health authorities.
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