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Title: Estrogen-dependent expression of sine oculis homeobox 1 in the mouse uterus during the estrous cycle

Journal Article · · Biochemical and Biophysical Research Communications
 [1];  [2];  [1];  [3]; ;  [1];  [4];  [1]
  1. Department of Biomedical Science, CHA University, Seongnam-si, Gyeonggi-do 13488 (Korea, Republic of)
  2. Fertility Center of CHA Bundang Medical Center, Seongnam-si, Gyeonggi-do 13496 (Korea, Republic of)
  3. Fertility Center of CHA Gangnam Medical Center, Seoul 06135 (Korea, Republic of)
  4. Department of Nanobiomedical Science & BK21 PLUS NBM Global Research Center for Regenerative Medicine, Dankook University, Cheonan-si, Chungcheongnam-do 31116 (Korea, Republic of)

The sine oculis homeobox 1 (SIX1) is a member of the Six gene family. SIX1 is involved in tissue development by regulating proliferation, apoptosis, and differentiation. However, function of SIX1 in the uterus remains unknown. Here, we found that Six1 expression is regulated along the estrous cycle in mouse uterus. Six1 expression was significantly increased at estrus stage and decreased at the rest of stages. SIX1 is detected in the luminal and glandular epithelium of uterine endometrium at the estrus stage. Estrogen injection increased Six1 expression in the ovariectomized mouse uterus, whereas progesterone had no effect on its expression. Estrogen receptor antagonist inhibited estrogen-induced Six1 expression. Our findings imply that SIX1 may play a role as an important regulator to orchestrate the dynamic of uterine endometrium in response to estrogen level during the estrous cycle. These results will give us a better understanding of uterine biology. - Highlights: • Six1 expression is regulated during the estrous cycle in mouse uterus. • Six1 is highly expressed at the estrus stage of estrous cycle. • SIX1 is detected in luminal/glandular epithelium of the uterus at the estrus stage. • Estrogen stimulates Six1 expression in an estrogen receptor-dependent manner.

OSTI ID:
22596321
Journal Information:
Biochemical and Biophysical Research Communications, Vol. 472, Issue 3; Other Information: Copyright (c) 2016 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
Country of Publication:
United States
Language:
English