Linli Hu1, Haixia Li2, CindyTzu-Ling Huang3, Hong Chen3, Guijin Zhu4, Kun Qian5. 1. Reproductive Medicine Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, People's Repubic of China; Reproductive Medicine Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Repubic of China. 2. Reproductive Medicine Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Repubic of China; Reproductive Medicine Center, Guangzhou General Hospital, Guangzhou Military Command of the Chinese People's Liberation Army, Guangzhou, People's Repubic of China. 3. Waisman Center, University of Wisconsin, Madison, Wisconsin. 4. Reproductive Medicine Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Repubic of China. 5. Reproductive Medicine Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Repubic of China. Electronic address: qk1129@tjh.tjmu.edu.cn.
Abstract
OBJECTIVE: To identify the expression profile and sex steroid regulation pattern of myeloid ecotropic viral integration site 1 (MEIS1) in endometrium. DESIGN: Molecular studies in human and animal tissue. SETTING: 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). INTERVENTION(S): 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. RESULT(S): 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. CONCLUSION(S): 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.
OBJECTIVE: To identify the expression profile and sex steroid regulation pattern of myeloid ecotropic viral integration site 1 (MEIS1) in endometrium. DESIGN: Molecular studies in human and animal tissue. SETTING: 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). INTERVENTION(S): 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. RESULT(S): 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. CONCLUSION(S): 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.
Authors: Eric M Erkenbrack; Jamie D Maziarz; Oliver W Griffith; Cong Liang; Arun R Chavan; Mauris C Nnamani; Günter P Wagner Journal: PLoS Biol Date: 2018-08-24 Impact factor: 8.029