Ciliated epithelial-specific and regional-specific expression and regulation of the estrogen receptor-β2 in the fallopian tubes of immature rats:: a possible mechanism for estrogen-mediated transport process in vivo

Several ER beta isoforms have been identified in human and rodent tissues, but it is unclear whether each isoform has distinctly different cellular targeting characteristics and physiological functions. We have investigated the intracellular localization and regulatory patterns for ER beta isoforms in rat fallopian tubes. Western blot analysis reveals that two ER beta isoforms corresponding to ER beta 1 and ER beta 2 are expressed in rat fallopian tubes. However, ER beta 2 is the predominant form of ER beta in this tissue. High-resolution confocal imaging and immunolustochemical analysis provide ample evidence that ER beta expression is limited almost exclusively to the ciliated epithelial cells, in contrast to ER alpha, which is widely distributed. Furthermore, within the ciliated epithelial cells, ER beta is colocalized with beta-tubulm IV at stem portion of the cilia. We show that ER beta 2 protein expression is tightly regulated by E2 or DPN in a time-dependent manner without changes in ER beta 1 expression. These estrogenic effects are inhibited by an ER antagonist, ICI 182,780. In addition, significant alteration of ER beta inummoreactivity is detected only histologically in the ampullary region. Since the cilia are considered an essential determinant of tubal transport, we further demonstrate that E(2)- or DPN-induced ER beta 2 activation is associated with alterations in tubal protein expression crucial for the regulation of calcium-dependent ciliary beating. Given the coordinated regulation and interaction of ER and progesterone receptor in the cilia, we hypothesize that tubal ER beta 2 may facilitate the estrogen-mediated transport process by processing protein-protein interaction under physiological and/or pathological conditions. We show for the first time that a previously unrecognized localization of ER beta isoform in rat fallopian tubes can combine with estrogen to individually control the expression of ER beta-isoforms in normal target tissues.