Increased pituitary vascular endothelial growth factor-A in dopaminergic D2 receptor knockout female mice
Vascular endothelial growth factor (VEGF)-A is an important angiogenic cytokine in cancer and pathological angiogenesis and has been related to the antiangiogenic activity of dopamine in endothelial cells. We investigated VEGF expression, localization, and function in pituitary hyperplasia of dopami...
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todo:paper_00137227_v146_n7_p2952_Cristina2023-10-03T14:11:17Z Increased pituitary vascular endothelial growth factor-A in dopaminergic D2 receptor knockout female mice Cristina, C. Díaz-Torga, G. Baldi, A. Góngora, A. Rubinstein, M. Low, M.J. Becú-Villalobos, D. 3 (4,5 dimethylthiazol 2 yl) 5 (3 carboxymethoxyphenyl) 2 (4 sulfophenyl) 2h tetrazolium cell nucleus antigen dopamine 2 receptor dopamine 2 receptor blocking agent estrogen haloperidol messenger RNA prolactin tetrazolium thymidine tritium unclassified drug vasculotropin A dopamine 2 receptor dopamine receptor blocking agent drug derivative estrogen haloperidol haloperidol decanoate prolactin vasculotropin A angiogenesis animal cell animal experiment animal model animal tissue antigen expression article cell proliferation comparative study confocal laser microscopy controlled study correlation analysis female genotype hyperplasia hypophysis cell immunofluorescence test in vitro study in vivo study knockout mouse mouse nonhuman paracrine signaling priority journal prolactin release protein expression protein localization stellate cell umbilical vein wild type animal blood cell culture chemistry culture medium cytology drug effect genetics human hypophysis metabolism mouse mutant pathology tissue distribution Animals Cell Proliferation Cells, Cultured Culture Media, Conditioned Dopamine Antagonists Estrogens Female Haloperidol Humans Hyperplasia Mice Mice, Knockout Pituitary Gland Prolactin Receptors, Dopamine D2 RNA, Messenger Tissue Distribution Umbilical Veins Vascular Endothelial Growth Factor A Vascular endothelial growth factor (VEGF)-A is an important angiogenic cytokine in cancer and pathological angiogenesis and has been related to the antiangiogenic activity of dopamine in endothelial cells. We investigated VEGF expression, localization, and function in pituitary hyperplasia of dopamine D2 receptor (D2R)-knockout female mice. Pituitaries from knockout mice showed increased protein and mRNA VEGF-A expression when compared with wild-type mice. In wild-type mice, prolonged treatment with the D2R antagonist, haloperidol, enhanced pituitary VEGF expression and prolactin release, suggesting that dopamine inhibits pituitary VEGF expression. VEGF expression was also increased in pituitary cells from knockout mice, even though these cells proliferated less in vitro when compared with wild-type cells, as determined by 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl) -2H-tetrazolium proliferation assay, proliferating cell nuclear antigen expression, and [3H]thymidine incorporation. In contrast to other animal models, estrogen did not increase pituitary VEGF protein and mRNA expression and lowered serum prolactin secretion in vivo and in vitro in both genotypes. VEGF(10 and 30 ng/ml) did not modify pituitary cell proliferation in either genotype and increased prolactin secretion in vitro in estrogen-pretreated cells of both genotypes. But conditioned media from D2R -/- cells enhanced human umbilical vein cell proliferation, and this effect could be partially inhibited by an anti-VEGF antiserum. Finally, using dual-labeling immunofluorescence and confocal laser microscopy, we found that in the hyperplastic pituitaries, VEGF-A was mostly present in follicle-stellate cells. In conclusion, pituitary VEGF expression is under dopaminergic control, and even though VEGF does not promote pituitary cellular proliferation in vitro, it may be critical for pituitary angiogenesis through paracrine actions in the D2R knockout female mice. Copyright © 2005 by The Endocrine Society. JOUR info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_00137227_v146_n7_p2952_Cristina |
institution |
Universidad de Buenos Aires |
institution_str |
I-28 |
repository_str |
R-134 |
collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
topic |
3 (4,5 dimethylthiazol 2 yl) 5 (3 carboxymethoxyphenyl) 2 (4 sulfophenyl) 2h tetrazolium cell nucleus antigen dopamine 2 receptor dopamine 2 receptor blocking agent estrogen haloperidol messenger RNA prolactin tetrazolium thymidine tritium unclassified drug vasculotropin A dopamine 2 receptor dopamine receptor blocking agent drug derivative estrogen haloperidol haloperidol decanoate prolactin vasculotropin A angiogenesis animal cell animal experiment animal model animal tissue antigen expression article cell proliferation comparative study confocal laser microscopy controlled study correlation analysis female genotype hyperplasia hypophysis cell immunofluorescence test in vitro study in vivo study knockout mouse mouse nonhuman paracrine signaling priority journal prolactin release protein expression protein localization stellate cell umbilical vein wild type animal blood cell culture chemistry culture medium cytology drug effect genetics human hypophysis metabolism mouse mutant pathology tissue distribution Animals Cell Proliferation Cells, Cultured Culture Media, Conditioned Dopamine Antagonists Estrogens Female Haloperidol Humans Hyperplasia Mice Mice, Knockout Pituitary Gland Prolactin Receptors, Dopamine D2 RNA, Messenger Tissue Distribution Umbilical Veins Vascular Endothelial Growth Factor A |
spellingShingle |
3 (4,5 dimethylthiazol 2 yl) 5 (3 carboxymethoxyphenyl) 2 (4 sulfophenyl) 2h tetrazolium cell nucleus antigen dopamine 2 receptor dopamine 2 receptor blocking agent estrogen haloperidol messenger RNA prolactin tetrazolium thymidine tritium unclassified drug vasculotropin A dopamine 2 receptor dopamine receptor blocking agent drug derivative estrogen haloperidol haloperidol decanoate prolactin vasculotropin A angiogenesis animal cell animal experiment animal model animal tissue antigen expression article cell proliferation comparative study confocal laser microscopy controlled study correlation analysis female genotype hyperplasia hypophysis cell immunofluorescence test in vitro study in vivo study knockout mouse mouse nonhuman paracrine signaling priority journal prolactin release protein expression protein localization stellate cell umbilical vein wild type animal blood cell culture chemistry culture medium cytology drug effect genetics human hypophysis metabolism mouse mutant pathology tissue distribution Animals Cell Proliferation Cells, Cultured Culture Media, Conditioned Dopamine Antagonists Estrogens Female Haloperidol Humans Hyperplasia Mice Mice, Knockout Pituitary Gland Prolactin Receptors, Dopamine D2 RNA, Messenger Tissue Distribution Umbilical Veins Vascular Endothelial Growth Factor A Cristina, C. Díaz-Torga, G. Baldi, A. Góngora, A. Rubinstein, M. Low, M.J. Becú-Villalobos, D. Increased pituitary vascular endothelial growth factor-A in dopaminergic D2 receptor knockout female mice |
topic_facet |
3 (4,5 dimethylthiazol 2 yl) 5 (3 carboxymethoxyphenyl) 2 (4 sulfophenyl) 2h tetrazolium cell nucleus antigen dopamine 2 receptor dopamine 2 receptor blocking agent estrogen haloperidol messenger RNA prolactin tetrazolium thymidine tritium unclassified drug vasculotropin A dopamine 2 receptor dopamine receptor blocking agent drug derivative estrogen haloperidol haloperidol decanoate prolactin vasculotropin A angiogenesis animal cell animal experiment animal model animal tissue antigen expression article cell proliferation comparative study confocal laser microscopy controlled study correlation analysis female genotype hyperplasia hypophysis cell immunofluorescence test in vitro study in vivo study knockout mouse mouse nonhuman paracrine signaling priority journal prolactin release protein expression protein localization stellate cell umbilical vein wild type animal blood cell culture chemistry culture medium cytology drug effect genetics human hypophysis metabolism mouse mutant pathology tissue distribution Animals Cell Proliferation Cells, Cultured Culture Media, Conditioned Dopamine Antagonists Estrogens Female Haloperidol Humans Hyperplasia Mice Mice, Knockout Pituitary Gland Prolactin Receptors, Dopamine D2 RNA, Messenger Tissue Distribution Umbilical Veins Vascular Endothelial Growth Factor A |
description |
Vascular endothelial growth factor (VEGF)-A is an important angiogenic cytokine in cancer and pathological angiogenesis and has been related to the antiangiogenic activity of dopamine in endothelial cells. We investigated VEGF expression, localization, and function in pituitary hyperplasia of dopamine D2 receptor (D2R)-knockout female mice. Pituitaries from knockout mice showed increased protein and mRNA VEGF-A expression when compared with wild-type mice. In wild-type mice, prolonged treatment with the D2R antagonist, haloperidol, enhanced pituitary VEGF expression and prolactin release, suggesting that dopamine inhibits pituitary VEGF expression. VEGF expression was also increased in pituitary cells from knockout mice, even though these cells proliferated less in vitro when compared with wild-type cells, as determined by 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl) -2H-tetrazolium proliferation assay, proliferating cell nuclear antigen expression, and [3H]thymidine incorporation. In contrast to other animal models, estrogen did not increase pituitary VEGF protein and mRNA expression and lowered serum prolactin secretion in vivo and in vitro in both genotypes. VEGF(10 and 30 ng/ml) did not modify pituitary cell proliferation in either genotype and increased prolactin secretion in vitro in estrogen-pretreated cells of both genotypes. But conditioned media from D2R -/- cells enhanced human umbilical vein cell proliferation, and this effect could be partially inhibited by an anti-VEGF antiserum. Finally, using dual-labeling immunofluorescence and confocal laser microscopy, we found that in the hyperplastic pituitaries, VEGF-A was mostly present in follicle-stellate cells. In conclusion, pituitary VEGF expression is under dopaminergic control, and even though VEGF does not promote pituitary cellular proliferation in vitro, it may be critical for pituitary angiogenesis through paracrine actions in the D2R knockout female mice. Copyright © 2005 by The Endocrine Society. |
format |
JOUR |
author |
Cristina, C. Díaz-Torga, G. Baldi, A. Góngora, A. Rubinstein, M. Low, M.J. Becú-Villalobos, D. |
author_facet |
Cristina, C. Díaz-Torga, G. Baldi, A. Góngora, A. Rubinstein, M. Low, M.J. Becú-Villalobos, D. |
author_sort |
Cristina, C. |
title |
Increased pituitary vascular endothelial growth factor-A in dopaminergic D2 receptor knockout female mice |
title_short |
Increased pituitary vascular endothelial growth factor-A in dopaminergic D2 receptor knockout female mice |
title_full |
Increased pituitary vascular endothelial growth factor-A in dopaminergic D2 receptor knockout female mice |
title_fullStr |
Increased pituitary vascular endothelial growth factor-A in dopaminergic D2 receptor knockout female mice |
title_full_unstemmed |
Increased pituitary vascular endothelial growth factor-A in dopaminergic D2 receptor knockout female mice |
title_sort |
increased pituitary vascular endothelial growth factor-a in dopaminergic d2 receptor knockout female mice |
url |
http://hdl.handle.net/20.500.12110/paper_00137227_v146_n7_p2952_Cristina |
work_keys_str_mv |
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