4.3 Article

Coexpression and Estrogen-Mediated Regulation of TRPV6 and PMCA1 in the Human Endometrium During the Menstrual Cycle

Journal

MOLECULAR REPRODUCTION AND DEVELOPMENT
Volume 78, Issue 4, Pages 274-282

Publisher

WILEY-BLACKWELL
DOI: 10.1002/mrd.21303

Keywords

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Funding

  1. National Research Foundation of Korea (NRF) from the Korea government (MEST) [2010-0011433]
  2. Korea government (MEST) [2010-0011433]

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Maintenance of calcium balance in the uterus is essential for many of its functions, including embryo implantation. The plasma membrane Ca2+-pumping ATPase proteins are encoded by four genes designated PMCA1-4, and PMCA1 is expressed in the uterus of rats during the estrous cycle. Although transient receptor potential cation channel subfamily V, member 6 (TRPV6), has been detected in the human placenta, pancreas and the prostate gland, expression patterns of uterine TRPV6 and PMCA1 and their potential roles in the human endometrium remain to be elucidated. In the present study, the expression patterns of TRPV6 and PMCA1 were examined to predict their potential roles in the human endometrium during the menstrual cycle. Human classified endometrial tissues (total n = 40) were separated into three groups according to menstrual cycle phase: menstrual, proliferative (early-, mid-, late), and secretory phase (early-, mid-, late). The expression of TRPV6 and PMCA1 mRNA and protein in the uterine endometrium during the menstrual cycle increased by 1.5- to 1.8-fold at the proliferative phase (early-, mid-, and late-) in comparison to the other phases. Estrogen treatment caused a significant increase in TRPV6 and PMCA1 mRNA expression. Immunohistochemical analysis of the distribution of TRPV6 and PMCA1 in the uterus revealed that both proteins are abundantly expressed in the cytoplasm of endometrial and glandular epithelial cells during menstrual phases. Taken together, these results suggest that uterine expression of TRPV6 and PMCA1 may be involved in human reproductive function. Mol. Reprod. Dev. 78: 274-282, 2011. (C) 2011 Wiley-Liss, Inc.

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