This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Seo, K. H. Articles by Im, S.-Y. Search for Related Content PubMed PubMed Citation Articles by Seo, K. H. Articles by Im, S.-Y.

Estrogen Enhances Angiogenesis through a Pathway Involving Platelet-Activating Factor-Mediated Nuclear Factor-B Activation

¹ Department of Biological Sciences, The Institute of Basic Sciences, Hormone Research Center, Chonnam National University, Kwangju, and ² Department of Immunology and Research Center for Allergic Immune Diseases, Chonbuk National University Medical School, Chonju, Republic of Korea

In this study, we investigated the molecular events involved in estrogen-induced angiogenesis. Treatment of the human endometrial adenocarcinoma cells, HEC-1A, with estrogen up-regulated mRNA expression and protein synthesis of various angiogenic factors such as tumor necrosis factor-, interleukin-1, basic fibroblast growth factor, and vascular endothelial growth factor. The estrogen-dependent induction of the expression was blocked by the platelet-activating factor (PAF) antagonists, WEB 2170. Estrogen treatment caused the activation of nuclear factor (NF)-B in HEC-1A cells and was also blocked by PAF antagonist. Inhibitors of NF-B activation inhibited estrogen-induced mRNA expression and protein synthesis of the angiogenic factors. Estrogen led to a pronounced angiogenesis as assessed by a mouse Matrigel model in vivo and endothelial cell sprouting in vitro. PAF antagonists or NF-B inhibitors significantly inhibited this estrogen-dependent angiogenesis. Estrogen caused phospholipase A₂ (PLA₂) gene and protein expression. Estrogen-induced vascular endothelial growth factor mRNA expression and sprouting were significantly inhibited by PLA₂ inhibitors, suggesting PLA₂ expression is the upstream pathway in the estrogen-induced angiogenesis. Taken together, these results suggest that estrogen induces the production of angiogenic factors via a mechanism involving PAF-mediated NF-B activation.

This article has been cited by other articles:

				C. Van Themsche, L. Lafontaine, and E. Asselin X-Linked Inhibitor of Apoptosis Protein Levels and Protein Kinase C Activity Regulate the Sensitivity of Human Endometrial Carcinoma Cells to Tumor Necrosis Factor{alpha}-Induced Apoptosis Endocrinology, August 1, 2008; 149(8): 3789 - 3798. [Abstract] [Full Text] [PDF]

				S. Doublier, M. Ceretto, E. Lupia, S. Bravo, B. Bussolati, and G. Camussi The Proangiogenic Phenotype of Tumor-Derived Endothelial Cells is Reverted by the Overexpression of Platelet-Activating Factor Acetylhydrolase Clin. Cancer Res., October 1, 2007; 13(19): 5710 - 5718. [Abstract] [Full Text] [PDF]

				O. V. Glinskii, T. W. Abraha, J. R. Turk, L. J. Rubin, V. H. Huxley, and V. V. Glinsky Microvascular network remodeling in dura mater of ovariectomized pigs: role for angiopoietin-1 in estrogen-dependent control of vascular stability Am J Physiol Heart Circ Physiol, August 1, 2007; 293(2): H1131 - H1137. [Abstract] [Full Text] [PDF]

				Y. B. Wetherill, J. K. Hess-Wilson, C. E.S. Comstock, S. A. Shah, C. R. Buncher, L. Sallans, P. A. Limbach, S. Schwemberger, G. F. Babcock, and K. E. Knudsen Bisphenol A facilitates bypass of androgen ablation therapy in prostate cancer Mol. Cancer Ther., December 1, 2006; 5(12): 3181 - 3190. [Abstract] [Full Text] [PDF]

				F. Wieser, J.-L. Vigne, I. Ryan, D. Hornung, S. Djalali, and R. N. Taylor Sulindac Suppresses Nuclear Factor-{kappa}B Activation and RANTES Gene and Protein Expression in Endometrial Stromal Cells from Women with Endometriosis J. Clin. Endocrinol. Metab., December 1, 2005; 90(12): 6441 - 6447. [Abstract] [Full Text] [PDF]