Differential Expression of the Motin Family in the Peri-implantation Mouse Uterus and Their Hormonal Regulation

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  • MATSUMOTO Hiromichi
    Laboratory of Animal Breeding and Reproduction, Division of Animal Science, Faculty of Agriculture, Utsunomiya University, Tochigi 321-8505, Japan
  • FUKUI Emiko
    Laboratory of Animal Breeding and Reproduction, Division of Animal Science, Faculty of Agriculture, Utsunomiya University, Tochigi 321-8505, Japan
  • YOSHIZAWA Midori
    Laboratory of Animal Breeding and Reproduction, Division of Animal Science, Faculty of Agriculture, Utsunomiya University, Tochigi 321-8505, Japan
  • SATO Eimei
    Laboratory of Animal Reproduction, Graduate School of Agricultural Science, Tohoku University, Sendai 981-8555, Japan
  • DAIKOKU Takiko
    Division of Reproductive Sciences, Perinatal Institute, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, OH 45229, USA

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Abstract

Increased vascular permeability and angiogenesis are hallmarks of the implantation process in the uterus. Angiomotin (Amot), which is a vascular angiogenesis-related protein, belongs to the motin family. There are two other members of the motin family, angiomotin-like 1 and 2 (Amotl1 and 2), which are also thought to be involved with angiogenesis. In the present study, the distribution of motin mRNAs in the mouse uterus during the peri-implantation period was investigated by in situ hybridization. Amot and Amotl1 were expressed in the stromal cells on days 3 and 4; expressions of Amotl2 during the same period were low. During the postimplantation period, Amot and Amotl1 were expressed in secondary decidual cells, while Amotl2 expression fell to an undetectable level. We also examined hormonal regulation of motin expression by steroid hormone treatment in ovariectomized mice. We found that expression of Amot was induced by P4 in stromal cells. Additionally, Amotl1 expression was upregulated by both P4 and estrogen (E2) in stromal cells, whereas E2 increased this gene expression for only a limited time; after 12 h, expression dissipated. In contrast, P4 regulated the expression of Amotl2 in stromal cells, while E2 regulated its expression in luminal epithelium cells. Our results demonstrated that Amot, Amotl1, and Amotl2 were differentially expressed in uterine cells during the peri-implantation period, and that their expressions were differentially regulated by P4 and E2.

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