Enhancement of apoptotic susceptibility by interleukin-1 beta in human endometrial epithelial cells

Gynecol Endocrinol. 1998 Oct;12(5):315-9. doi: 10.3109/09513599809012832.

Abstract

Interleukin-1 (IL-1) is considered to be an essential cytokine for embryonic implantation. Expression of the IL-1 receptor in endometrial luminal epithelium increases maximally in the peri-implantation period, and embryonic implantation in mice is blocked by the IL-1 receptor antagonist. However, the function of IL-1 alone in implantation is still unclear. It has been reported that endometrial epithelial cells undergo apoptosis at the implantation site. In this study we have investigated the regulatory function of IL-1 in endometrial epithelial apoptosis, using the human endometrial epithelial cell line HHUA, which is susceptible to Fas-mediated apoptosis. The enhancement of endometrial apoptosis by IL-1 beta was not accompanied by any increase in cell-surface expression of Fas, which suggested that IL-1 beta enhanced the postreceptor apoptotic signals in the activated cells. IL-1 may be a regulator of apoptotic susceptibility in endometrial epithelium in the peri-implantation period.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenocarcinoma
  • Animals
  • Apoptosis*
  • Cell Division
  • DNA Fragmentation
  • Endometrial Neoplasms
  • Endometrium / cytology
  • Endometrium / metabolism*
  • Epithelial Cells / metabolism
  • Female
  • Flow Cytometry
  • Humans
  • Interleukin-1 / metabolism*
  • Mice
  • Receptors, Interleukin-1 / antagonists & inhibitors*
  • Tumor Cells, Cultured

Substances

  • Interleukin-1
  • Receptors, Interleukin-1