Genetically Induced Estrogen Receptor α mRNA (Esr1) Overexpression Does Not Adversely Affect Fertility or Penile Development in Male Mice

• Published in: Journal of andrology 2011-05, Vol.32 (3), p.282-294
• Main Authors: Heath, John, Abdelmageed, Yazeed, Braden, Tim D., Williams, Carol S., Williams, John W., Paulose, Tessie, Hernandez‐Ochoa, Isabel, Gupta, Rupesh, Flaws, Jodi A., Goyal, Hari O.
• Format: Article
• Language: English
• Subjects: Animals; Base Sequence; Biological and medical sciences; Blotting, Western; Body Weight; DNA Primers; Estrogen Receptor alpha - genetics; Female; Fertility - genetics; Fundamental and applied biological sciences. Psychology; Gynecology. Andrology. Obstetrics; Male; Male genital diseases; Mammalian male genital system; Medical sciences; Mice; Mice, Transgenic; Mutant mice; Organ Size; penis; Penis - embryology; Polymerase Chain Reaction; Rats; RNA, Messenger - genetics; seminal vesicles; testis; Testosterone - blood; Testosterone - metabolism; Vertebrates: reproduction
• ISSN: 0196-3635; 1939-4640
• DOI: 10.2164/jandrol.110.010769

Previously, we reported that estrogen receptor α mRNA (Esr1) or protein (ESR1) overexpression resulting from neonatal exposure to estrogens in rats was associated with infertility and maldeveloped penis characterized by reduced length and weight and abnormal accumulation of fat cells. The objective of this study was to determine if mutant male mice overexpressing Esr1 are naturally infertile or have reduced fertility and/or develop abnormal penis. The fertility parameters, including fertility and fecundity indices, numbers of days from the day of cohabitation to the day of delivery, and numbers of pups per female, were not altered from controls as a result of Esr1 overexpression. Likewise, penile morphology, including the length, weight, and diameter and os penis development, was not altered from controls. Conversely, weights of the seminal vesicles and bulbospongiosus and levator ani (BS/LA) muscles were significantly (P < .05) lower as compared with controls; however, the weight of the testis, the morphology of the testis and epididymis, and the plasma and testicular testosterone concentration were not different from controls. Hence, genetically induced Esr1 overexpression alone, without an exogenous estrogen exposure during the neonatal period, is unable to adversely affect the development of the penis as well as other male reproductive organs, except for limited, but significant, reductions in weights of the seminal vesicles and BS/LA muscles.