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Department of Clinical Physiopathology, Endocrinology Unit (C.C., P.F., R.M., M.S.) and Andrology Unit (M.Ma., S.G., M.Mu., G.F., M.L.); and Department of Anatomy, Histology, and Forensic Medicine (G.B.V.), University of Florence, I-50139 Florence, Italy
Address all correspondence and requests for reprints to: Michaela Luconi, Ph.D., Unità di Andrologia, Dipartimento di Fisiopatologia Clinica, Università di Firenze, Viale Pieraccini 6, I-50139 Florence, Italy. E-mail: m.luconi{at}dfc.unifi.it.
It is generally assumed that male genital development is determined by androgens on a default program leading to female genitalia. Female genitalia virilization is due to high levels of androgens, whereas feminization is linked to reduction or lack of fetal androgen. Excess androgen determines sex reversion in female, whereas excess estrogen does not cause male feminization. In the present study, we investigate the presence of androgen receptors (AR) and estrogen receptors (ER) in human fetal penile tissue and in a cellular model of human fetal penile smooth muscle cells (hfPSMC). By immunohistochemistry, we showed the presence of ER and AR in the developing penile tissue of male fetuses. Besides the presence of AR, hfPSMC showed ER
/ß as demonstrated by RT-PCR, Western blot, and binding techniques. These receptors are functionally active because cell stimulation with 17ß-estradiol increased progesterone receptor B expression and inhibited hfPSMC growth, both effects being reversed by tamoxifen. Conversely, cell proliferation was stimulated by R1881 and testosterone, an effect enhanced by letrozole. These findings are the first demonstration of the presence of functional ER in differentiating male external genitalia and indicate a possible novel inhibitory role of estrogens in the regulation of the development of these sex structures.
This study was supported by the University of Florence, Ministry of University and Scientific Research (Programmi di Ricerca Scientifica di Rilevante Interesse Nazionale), by Eli Lilly (Sesto Fiorentino, Italy), and by a grant of the Italian Public Health Institute (Rome, Italy).
Abbreviations: AR, Androgen receptor(s); CC, corpus cavernosum; DES, diethylstilbestrol; ER, estrogen receptor(s); FBS, fetal bovine serum; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; [3H]estradiol, [2,4,6,7,16,17-3H]estradiol; hfPSMC, human fetal penile smooth muscle cell(s); LNCaP, lymph node carcinoma of prostate; PR, progesterone receptor; T, testosterone.
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