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Center for Experimental Therapeutics and Department of Pharmacology, and Center for Research on Reproduction and Women’s Health, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104
Address all correspondence and requests for reprints to: W.-C. Song, Ph.D., University of Pennsylvania School of Medicine, Room 1351, Biomedical Research Building II/III, 421 Curie Boulevard, Philadelphia, Pennsylvania 19104. E-mail: . song{at}spirit.gcrc.upenn.edu
Estrogen sulfotransferase (EST) catalyzes the sulfoconjugation and inactivation of the steroid hormone estrogen. It is known previously that EST is expressed abundantly in Leydig cells of the testis. We recently have shown that male mice with targeted EST gene disruption developed age related Leydig cell and seminiferous tubule abnormalities as a consequence of increased local estrogen stimulation. In the same study, we also found that epididymal sperm isolated from the mutant mice had significantly reduced motility, but whether this reflected impaired epididymal function or was secondary to the testicular lesions was not known. The purpose of the current study was to investigate if EST is normally present in the mouse epididymis and/or other parts of the male reproductive tract where, as in testis, it may play a role in regulating local estrogen homeostasis. We describe here that EST is expressed in the epithelium of corpus and cauda but not caput regions of the mouse epididymis. It is also expressed in the luminal epithelium and smooth muscle cells of the vas deferens but was present at very low levels, if at all, in the prostate or seminal vesicle/ coagulating gland. Hypophysectomy, castration, and epididymal ligation experiments, together with the use of an androgen receptor antagonist, established that EST expression in the epididymis and vas deferens is critically dependent on pituitary hormone(s) and androgen but not on other factors in the testicular fluid. Administration of exogenous estradiol to mice with surgically ligated epididymis resulted in a more pronounced reduction in sperm motility in EST mutant mice than in wild-type mice. We conclude that EST is discretely expressed and regulated in the male reproductive tract and plays a physiological role in maintaining the functional integrity of the epididymis by regulating luminal estrogen homeostasis.
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  V. K. Khor, M. H. Tong, Y. Qian, and W.-C. Song Gender-Specific Expression and Mechanism of Regulation of Estrogen Sulfotransferase in Adipose Tissues of the Mouse Endocrinology, November 1, 2008; 149(11): 5440 - 5448. [Abstract] [Full Text] [PDF]
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K. De Gendt, N. Atanassova, K. A. L. Tan, L. R. de Franca, G. G. Parreira, C. McKinnell, R. M. Sharpe, P. T. K. Saunders, J. I. Mason, S. Hartung, et al. Development and Function of the Adult Generation of Leydig Cells in Mice with Sertoli Cell-Selective or Total Ablation of the Androgen Receptor Endocrinology, September 1, 2005; 146(9): 4117 - 4126. [Abstract] [Full Text] [PDF]
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M. H. Tong, L. K. Christenson, and W.-C. Song Aberrant Cholesterol Transport and Impaired Steroidogenesis in Leydig Cells Lacking Estrogen Sulfotransferase Endocrinology, May 1, 2004; 145(5): 2487 - 2497. [Abstract] [Full Text] [PDF]
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