Regulation of myeloid ecotropic viral integration site 1 and its expression in normal and abnormal endometrium
Myeloid ecotropic viral integration site 1 (MEIS1) was expressed in response to sex steroid in the endometrium both in vitro and in vivo. Diminished endometrium MEIS1 expression may contribute to implantation failure in endometriosis.
Linli Hu, M.D., Haixia Ni, M.D., Cindy Tzu-Ling Huang, Ph.D., Hong Chen, M.D., Guijin Zhu, M.D., Kun Qian, M.D.
Volume 102, Issue 3, Pages 856-863
To identify the expression profile and sex steroid regulation pattern of myeloid ecotropic viral integration site 1 (MEIS1) in endometrium.
Molecular studies in human and animal tissue.
Reproductive medicine center of a university hospital.
Patient(s) and Animal(s):
Women with normal menstrual cycles for male infertility and female infertility with endometriosis. Sexually mature female mice (Kunming White strain).
Primary cultured endometrial stromal cells, Ishikawa cells, and oophorectomized mice were treated with sex steroid.
Main Outcome Measure(s):
MEIS1 expression in the human endometrium during the menstrual cycle, mouse uterus during the peri-implantation period of pregnancy, and eutopic endometrium from patients with endometriosis was analyzed by immunohistochemistry staining and western blot. In addition, MEIS1 expression in response to sex steroid was examined both in vitro and in vivo by immunohistochemistry staining and western blot.
MEIS1 expression was markedly increased in endometrium during the implantation period, and in decidualizing stromal cells in human endometrium and murine uterus. Steroid hormones increased MEIS1 expression in primary cultured endometrial stromal cells, Ishikawa cells, and endometrium of oophorectomized mice. The effects of estrogen and progesterone were more marked in oophorectomized mice and were additive. MEIS1 expression was significantly lower in eutopic endometrium compared with normal endometrium in the midsecretory stage.
MEIS1 is likely a key mediator between sex steroid and genes for uterine receptivity. Diminished endometrium MEIS1 expression may contribute to implantation failure in endometriosis.