Gene expression profiles of the normal myometrium after 48 and 96 hours of exposure to BPA

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• 作者：So Yeon Kang ; Mee Ran Kim ; Jang Heub Kim ; Hyun Hee Cho
• 关键词：BPA ; Fibroid ; Myometrium ; Uterus
• 刊名：BioChip Journal
• 出版年：2015
• 出版时间：December 2015
• 年：2015
• 卷：9
• 期：4
• 页码：293-299
• 全文大小：345 KB
• 参考文献：1.Gould, J.C. et al. Bisphenol A interacts with the estrogen receptor a in a distinct manner from estradiol. Mol. Cell. Endocrinol. 142, 203–214 (1998).CrossRef
  2.Kuiper, G.G. et al. Interaction of estrogenic chemicals and phytoestrogens with estrogen receptor beta. Endocrinol. 139, 4252–4263 (1998).
  3.Pennie, W.D., Aldridge, T.C. & Brooks, A.N. Differential activation by xenoestrogens of ER a and ER ß when linked to different response elements. J. Endocrinol. 158, R11–R14 (1998).CrossRef
  4.Welshons, W.V., Nagel, S.C. & Saal. F.S. Large effects from small exposures, III. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. Endocrinol. 147, S56–S69 (2006).CrossRef
  5.Wetherill, Y.B. et al. In vitro molecular mechanisms of bisphenol A action. Reprod. Toxicol. 24, 178–198 (2007).CrossRef
  6.Takeuchi, T. & Tsutsumi, O. Serum bisphenol A concentrations showed gender differences, possibly linked to androgen levels. Biochem. Biophys. Res. Commun. 291, 76–78 (2002).CrossRef
  7.Takeuchi, T., Tsutsumi, O., Ikezuki, Y., Takai, Y. & Taketani, Y. Positive relationship between androgen and the endocrine disruptor, bisphenol A, in normal women and women with ovarian dysfunction. Endocr. J. 51, 165–169 (2004).CrossRef
  8.Yamada, H. et al. Maternal serum and amniotic fluid bisphenol A concentrations in the early second trimester. Reprod. Toxicol. 16, 735–739 (2002).CrossRef
  9.Sugiura-Ogasawara, M., Ozaki, Y., Sonta, S.I., Makino, T. & Suzumori, K. Exposure to bisphenol A is associated with recurrent miscarriage. Hum. Reprod. 20, 2325–2329 (2005).CrossRef
  10.Diamanti-Kandarakis, E. et al. Endocrine-Disrupting Chemicals: An Endocrine Society Scientific Statement. Endocr. Rev. 30, 293–342 (2009).CrossRef
  11.Kang, S.Y., Song, J.Y. & Cho H.H. Gene expression analysis of uterine smooth muscle cells exposed to bisphenol A, Toxicol. Environ. Health. Scien. 6, 261–267 (2014).
  12.Medikare, V., Kandukuri, L.R., Ananthapur, V., Deenadayal, M. & Nallari, P. The genetic bases of uterine fibroids; a review. J. Reprod. Infertil. 12, 181–91 (2011).
  13.Litovkin, K.V. et al. Microarray study of gene expression in uterine leiomyoma. Exp. Oncol. 30, 106–111 (2008).
  14.Leppert, P.C., Catherino, W.H. & Segars, J.H. A new hypothesis about the origin of uterine fibroids based on gene expression profiling with microarrays. Am. J. Obstet. Gynecol. 195, 415–420 (2006).CrossRef
  15.Flake, G.P., Andersen, J. & Dixon, D. Etiology and pathogenesis of uterine leiomyomas: a review. Environ. Health. Perspect. 111, 1037–1054 (2003).CrossRef
  16.Tsibris, J.S. et al. Insights from gene arrays on the development and growth regulation of uterine leiomyomata. Fertil. Steril. 78, 114–121 (2002).CrossRef
  17.Hoffman, P.J., Milliken, D.B., Gregg, L.C., Davis, R.R. & Gregg, J.P. Molecular characterization of uterine of pathogenesis. Fertil. Steril. 82, 639–649 (2004).CrossRef
  18.Vialle-Castellano, A. et al. Abundant expression of fibronectin is a major feature of leukemic dendritic cells differentiated from patients with acute myeloid leukemia. Leukemia. 18, 426–433 (2004).CrossRef
  19.Ciarmela, P. et al. Growth factors and myometrium: biological effects in uterine fibroid and possible clinical implications. Human. Reprod. Update. 17, 772–790 (2011).CrossRef
  20.Midwood, K.S. & Orend, G. The role of tenascin-C in tissue injury and tumorigenesis. J. Cell. Commun. Signal. 3, 287–310 (2009).CrossRef
  21.Orend, G. & Chiquet Ehrismann, R. Tenascin C induced signaling in cancer. Cancer Lett. 244, 143–163 (2006).CrossRef
  22.Imanaka-Yoshida, K., Joroe, M. & Yoshida, T. Interaction between cell and extracellular matrix in heart disease: multiple roles of tenascin-C in tissue remodeling. Histhol. Histopathol. 19, 517–525 (2004).
  23.Bogusiewicz, M. et al. Expression of matricellular proteins in human uterine leiomyomas and normal myometrium. Histol. Histopathol. 27, 1495–1502 (2012).
  24.Hennessy, B.T., Smith, D.L., Ram, P.T., Lu, Y. & Mills, G.B. Exploiting the PI3K/AKT pathway for cancer drug discovery. Nat. Rev. Drug. Discov. 4, 988–1004 (2005).CrossRef
  25.Datta, S.R., Brunet, A. & Greenberg, M.E. Celluar survival: a play in three AKTs. Genes. Dev. 13, 2905–2927 (1999).CrossRef
  26.Kovacs, K.A. et al. Differential expression of AKT/ protein kinase B, Bcl-2 and Bax proteins in human leiomyoma and myometrium. J. Steroid. Biochem. Mol. Biol. 87, 233–240 (2003).CrossRef
  27.Hoekstra, A.V. et al. Progestins activate the AKT pathway in leiomyoma cells and promote survival. J. Clin. Endocrinol. Metab. 94, 1768–1774 (2009).CrossRef
  28.Kawaguchi, K. et al. Mitotic activity in uterine leiomyomas during the menstrual cycle. Am. J. Obstet. Gynecol. 160, 637–641 (1989).CrossRef
  29.Vandenberg, L.N., Hauser, R., Marcus, M., Olea, N. & Welshons, W.V. Human exposure to bisphenol A. Reprod. Toxicol. 24, 139–177 (2007).CrossRef
  
• 作者单位：So Yeon Kang (1)
  Mee Ran Kim (1)
  Jang Heub Kim (1)
  Hyun Hee Cho (1)
  
  1. Department of Ob/Gyn, Seoul St. Mary’s Hospital, Catholic University Medical College, Banpo-dong, Seocho-gu, Seoul, 156-080, Korea
  
• 刊物类别：Chemistry and Materials Science
• 刊物主题：Chemistry
  Biotechnology
  
• 出版者：The Korean BioChip Society, in co-publication with Springer Verlag GmbH
• ISSN：2092-7843

文摘

Bisphenol A (BPA) is a plasticizer and affects estrogen metabolism and function. Because of its estrogenic activity, BPA may be the underlying cause of female estrogen-dependent tumors such as leiomyoma and endometriosis. In this investigation, we used microarrays to study the effects of BPA on RNA expression of normal uterine myometrial cells without estrogen condition. We previously determined that the expression of genes related to the formation of leiomyoma was altered after 48 h of BPA exposure. In order to determine if these changes depend on exposure time, uterine myometrial cells were cultured and treated with BPA for 48 and 96 h without estrogen. RNA extraction, microarray analysis, and quantitative polymerase chain reaction (qPCR) analysis were performed. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were used for evaluation of gene expression changes. The expression levels of genes related to the formation of fibroids changed after 48 h and 96 h, but these changes of gene expression did not show time depend manner. BPA doses not continuously alter the expression of genes in uterine smooth muscle cells without estrogen. These results suggest the action mechanism of BPA to change of gene expression might be related to the action of estrogen. Keywords BPA Fibroid Myometrium Uterus