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Obstetrics and Gynecology International
Volume 2013 (2013), Article ID 368543, 7 pages
http://dx.doi.org/10.1155/2013/368543
Research Article

Obesity and the Endometrium: Adipocyte-Secreted Proinflammatory TNFα Cytokine Enhances the Proliferation of Human Endometrial Glandular Cells

1Department of Obstetrics and Gynecology, Center for Women’s Health Research, Meharry Medical College, Nashville, TN 37208, USA
2Baylor College of Medicine, 1 Baylor Plaza, Houston, TX 77030, USA

Received 30 May 2013; Accepted 22 September 2013

Academic Editor: Eric Prossnitz

Copyright © 2013 Sangeeta Nair et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Obesity, a state of chronic inflammation, is associated with poor fertility and low implantation rates and is a well-documented risk factor for endometrial cancer. Adipokines, such as tumor necrosis factor alpha, play an important role in initiation of endometrial cancer. The aim of this study is to evaluate in vitro effects of human adipocyte cells (SW872) on growth of endometrial glandular epithelial cells (EGE). Methods. We measured cell proliferation and expression of cell-growth proteins—proliferating cell nuclear antigen, cyclin D1, cyclin-dependent kinase-1, and apoptotic markers (BCL-2 and BAK) in human EGE cells cocultured with SW872 cells. EGE cells were also evaluated in SW872-conditioned media neutralized with anti-TNFα antibody. Results. A significant increase in EGE cell proliferation was observed in both SW872-conditioned media and in coculture ( ). We observed an upregulation of proliferation markers PCNA, cyclin D1, CDK-1, and BCL-2 and decrease in BAK ( ). Neutralization of SW872-conditioned media using anti-TNFα antibodies reversed EGE cell proliferation as indicated by BCL-2 expression. Conclusions. Adipocytes have potent proliferative paracrine effect on EGE cells which may be, in part, mediated via TNFα. Further understanding of the role of obesity in endometrial carcinogenesis should lead to better preventative and therapeutic strategies.