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endothelium as a byproduct of the conversion of l -arginine, NADPH, and oxygen to l -citrulline, NADP + , and H + by the enzyme endothelial NO synthase (eNOS). Once formed, NO acutely acts on underlying vascular smooth muscle cells to reduce tension and so
INSERM, IFR105 Université Paris 7, INSERM, U553, Hémostase, Endothélium et Angiogénèse, Hôpital Saint Louis, 1 Avenue Claude Vellefaux, 75475 Paris Cedex 10, France
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INSERM, IFR105 Université Paris 7, INSERM, U553, Hémostase, Endothélium et Angiogénèse, Hôpital Saint Louis, 1 Avenue Claude Vellefaux, 75475 Paris Cedex 10, France
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INSERM, IFR105 Université Paris 7, INSERM, U553, Hémostase, Endothélium et Angiogénèse, Hôpital Saint Louis, 1 Avenue Claude Vellefaux, 75475 Paris Cedex 10, France
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INSERM, IFR105 Université Paris 7, INSERM, U553, Hémostase, Endothélium et Angiogénèse, Hôpital Saint Louis, 1 Avenue Claude Vellefaux, 75475 Paris Cedex 10, France
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Environmental chemicals may affect human health by disrupting endocrine function. Their possible role in the mammary gland and breast tumors is still unknown. Previous studies have demonstrated that vascular endothelial growth factor (VEGF), a key factor in angiogenesis and tumor progression, is an estrogen-regulated gene. We analyzed whether VEGF expression is regulated by different xenoestrogens in several breast cancer cells, MELN (derived from MCF-7) and MELP (derived from MDA-MB-231) and stably expressing estrogen receptor α (ERα); these cell lines stably express estrogen response element (β-globin)-luciferase. Genistein, bisphenol A (BPA), 4-(tert-octyl)phenol (OP), dieldrin, and several phthalates, including benzyl butyl phthalate (BBP) and di-ethyl-2-hexyle phthalate (DEHP), were first shown to be estrogenic. These compounds induced a dose-dependent increase of VEGF secretion in MELN and MCF-7 cells; maximal effect was observed at 1–10 μM non-cytotoxic concentrations and was inhibited by the antiestrogen ICI 182 780. VEGF increase was not observed in ERα-negative MDA-MB-231 cells. Most substances increased VEGF transcript levels in MELN cells. In contrast, γ-hexachlorocyclohexane, vinclozolin, and the phthalates (mono-n-butyl ester phthalic acid, di-isononyle phthalate, and di-isodecyle phthalate) were ineffective on both VEGF secretion and estrogenic luciferase induction in these cell lines. Specific kinase inhibitors PD98059, SB203580, or LY294002 suppressed the xenoestrogen-induced VEGF response, suggesting activation of MEK, p38 kinase, and phosphatidylinositol-3-kinase pathways. Our in vitro results show for the first time that genistein and xenoestrogens (BPA, OP, dieldrin, BBP, and DEHP at high concentrations) up-regulate VEGF expression in MELN cells by an ER-dependent mechanism. Since VEGF increases capillary permeability and breast tumor angiogenesis in vivo, the physiological relevance of these findings is discussed.
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aortic, carotid, mesenteric, pulmonary, renal, middle cerebral, and septal coronary arterial segments; 2) to assess the involvement of ERs in the vasorelaxing response to E 4 in uterine arteries; and 3) to assess the endothelium-dependent and endothelium
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or after incubation (as required by that particular experiment), the endothelium was removed by rubbing the intimal surface with a cotton swab. Successful denudation was confirmed by the absence of a relaxation to 10 −5 M acetylcholine. Strips were
Department of Veterinary Biomedical Sciences, University of Missouri, Columbia, Missouri 65211, USA
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Department of Veterinary Biomedical Sciences, University of Missouri, Columbia, Missouri 65211, USA
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Department of Veterinary Biomedical Sciences, University of Missouri, Columbia, Missouri 65211, USA
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Department of Veterinary Biomedical Sciences, University of Missouri, Columbia, Missouri 65211, USA
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Department of Veterinary Biomedical Sciences, University of Missouri, Columbia, Missouri 65211, USA
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Department of Veterinary Biomedical Sciences, University of Missouri, Columbia, Missouri 65211, USA
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vasomotor responses were determined for euthyroid and hypothyroid rats, endothelium-dependent dilation was also found to be blunted in isolated aortae ( Delp et al. 1995 , McAllister et al. 2000 ) and isolated perfused kidneys ( Vargas et al. 1995
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to the organ/organ system level. A growing body of evidence points to the disruption of these incompletely understood processes as potential mediators of the symptoms of PE. More specifically, although many studies point to the vascular endothelium as
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. 2000 ), arterial stiffness ( Smith et al. 2002 ), endothelial and/or endothelium-independent vasodilation ( Rossoni et al. 1999 , Evans et al. 2000 , Capaldo et al. 2001 ), and may reverse markers of early atherosclerosis ( Pfeifer et al
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.5; KCl, 4.6; KH 2 PO 4 , 1.2; MgSO 4 .7H 2 O, 1.2; NaHCO 3 , 25; glucose, 11.1; Na 2 EDTA, 0.03) at 4 °C. The endothelium was removed to eliminate the main source of vasoactive substances, including NO. This avoided possible actions on endothelial cells
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Unit of Clinical Pharmacology, Turku University Hospital, Turku, Finland
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–80% of the maximal reference contraction to KCl and endothelium-dependent vasodilatation response to acetylcholine was determined. Endothelium-independent relaxation was studied in a similar fashion using cumulative doses of sodium nitroprusside (SNP
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) cells of pancreatic islet and (B) the endothelium of pancreatic blood vessels. (C) Ovary was used as positive control. (D) Pancreatic tissue without the addition of primary antibody was used as negative control. Confocal microscopy of double
