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Articles by H. S. Taylor
Total Records ( 3 ) for H. S. Taylor
  H Sadeghi and H. S. Taylor

Expression of the GABAA receptor has been described previously in the human endometrium in both luminal epithelium and stroma. Its expression is increased during decidualization in rodents and in the implantation window of human endometrium. Here we localized GABA subunit receptor protein in human endometrium and identified regulators of gene expression and activation. GABAA was localized to the cell surface, and expression increased during the window of embryo implantation in human endometrium. The well-differentiated human endometrial adenocarcinoma cell line Ishikawa was treated with progesterone and transfected with pcDNA-HOXA10, HOXA10 siRNA, or respective controls. GABAA receptor mRNA expression was evaluated by real-time RT-PCR. Protein expression and localization were evaluated using immunofluorescence. GABAA receptor mRNA expression was increased significantly after either progesterone treatment or HOXA10 transfection. Coadministration of progesterone along with HOXA10 transfection had no additional effect on the expression of GABAA receptor mRNA over either agent alone. Blocking HOXA10 expression with siRNA prevented progesterone-induced GABAA receptor mRNA expression. Additionally, either HOXA10 or progesterone independently caused increased translocation of the GABA receptor from the cytoplasm to the cell membrane. Translocation in response to progesterone was blocked with HOXA10 siRNA. Progesterone-induced GABAA subunit receptor expression is likely mediated indirectly through progesterone's regulation of HOXA10 expression. Modification of subtype composition and translocation of the GABA receptor ion channel likely modulate endometrial receptivity. Whereas HOXA10 typically enhances the expression of progesterone-responsive genes, here HOXA10 expression leads to production of a less progestin-responsive GABA receptor subtype, likely buffering the effects of luteal phase progesterone on GABA receptor activity.

  J. G Bromer , J Wu , Y Zhou and H. S. Taylor

Diethylstilbestrol (DES) is a nonsteroidal estrogen that induces developmental anomalies of the female reproductive tract. The homeobox gene HOXA10 controls uterine organogenesis, and its expression is altered after in utero DES exposure. We hypothesized that an epigenetic mechanism underlies DES-mediated alterations in HOXA10 expression. We analyzed the expression pattern and methylation profile of HOXA10 after DES exposure. Expression of HOXA10 is increased in human endometrial cells after DES exposure, whereas Hoxa10 expression is repressed and shifted caudally from its normal location in mice exposed in utero. Cytosine guanine dinucleotide methylation frequency in the Hoxa10 intron was higher in DES-exposed offspring compared with controls (P = 0.017). The methylation level of Hoxa10 was also higher in the caudal portion of the uterus after DES exposure at the promoter and intron (P < 0.01). These changes were accompanied by increased expression of DNA methyltransferases 1 and 3b. No changes in methylation were observed after in vitro or adult DES exposure. DES has a dual mechanism of action as an endocrine disruptor; DES functions as a classical estrogen and directly stimulates HOXA10 expression with short-term exposure, however, in utero exposure results in hypermethylation of the HOXA10 gene and long-term altered HOXA10 expression. We identify hypermethylation as a novel mechanism of DES-induced altered developmental programming.

  J Sarno , F Schatz , S. J Huang , C Lockwood and H. S. Taylor

Bleeding or inflammation in early pregnancy may result in pregnancy loss or defective implantation. Their effect on HOX gene expression in first trimester decidua is unknown. Bleeding results in thrombin generation, although infection or inflammation results in production of cytokines typified by Interleukin-1β (IL-1β). First trimester decidual cells were pretreated with 17β estradiol (E2), medroxyprogesterone acetate (MPA) or both and subsequently treated with thrombin or IL-1β. Affymetrix microarray analysis was used to assess the expression of all HOX genes and confirmed using real-time RT–PCR. E2 or MPA treatment resulted in significant increases in HOXA10 and HOXA11. Subsequent treatment with thrombin resulted in diminished expression of HOXA10 and HOXA9. Treatment with IL-1β resulted in decreased expression of HOXA1, 3, 9, 10 and 11. HOXA10 expression was reduced by 70% after thrombin treatment (P = 0.018) and by 90% after IL-1β treatment (P = 0.004). HOXA11 mRNA expression was decreased by 88% after IL-1β treatment (P < 0.001), but not by thrombin treatment. Decidua was collected at the time of elective termination of pregnancy (n = 10) or surgical treatment of spontaneous pregnancy loss (n = 10). Real-time PCR and western analysis demonstrated decreased HOXA10 and HOXA11 RNA and protein expression in the decidua of spontaneous pregnancy loss compared with that of viable pregnancies. In conclusion, multiple HOX genes are expressed in decidual cells and inhibited by thrombin and IL-1β. Since HOXA10 and HOXA11 are known to be necessary for successful pregnancy, these findings suggest a molecular mechanism by which bleeding or inflammation may affect pregnancy outcome.

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