title: Disruption of aryl hydrocarbon receptor (AhR) induces regression of the seminal vesicle in aged male mice.
abstract: The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that mediates diverse dioxin toxicities. Despite mediating the adverse effects, the AhR gene is conserved among animal species, suggesting important physiological functions for AhR. In fact, a recent study revealed that AhR has an intrinsic function in female reproduction, though its role in male reproduction is largely unknown. In this study, we show age-dependent regression of the seminal vesicles, probably together with the coagulating gland, in AhR(-/-) male mice. Knockout mice had abnormal vaginal plugs, low sperm counts in the epididymis, and low fertility. Moreover, serum testosterone concentrations and expression of steroidogenic 3betahydroxysteroiddehydrogenase (3betaHsd) and steroidogenic acute regulatory protein (StAR) in testicular Leydig cells were decreased in AhR(-/-) males. Taken together, our results suggest that impaired testosterone synthesis in aged mice induces regression of seminal vesicles and the coagulating glands. Such tissue disappearance likely resulted in abnormal vaginal plug formation, and eventually in low fertility. Together with previous findings demonstrating AhR function in female reproduction, AhR has essential functions in animal reproduction in both sexes.
authors.affiliation: Division of Sex Differentiation, National Institute for Basic Biology, National Institutes of Natural Sciences, Higashiyama, Myodaiji-cho, Okazaki, Aichi, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Baba
authors.forename: Y
authors.initials: Y
authors.lastname: Shima
authors.forename: A
authors.initials: A
authors.lastname: Owaki
authors.forename: J
authors.initials: J
authors.lastname: Mimura
authors.forename: M
authors.initials: M
authors.lastname: Oshima
authors.forename: Y
authors.initials: Y
authors.lastname: Fujii-Kuriyama
authors.forename: K-i
authors.initials: KI
authors.lastname: Morohashi
mesh_terms: D015096:3-Hydroxysteroid Dehydrogenases / Q000378:metabolism; D000375:Aging / Q000502:physiology*; D000818:Animals; D015153:Blotting, Western; D005260:Female; D007150:Immunohistochemistry; D007985:Leydig Cells / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009845:Oligospermia / Q000503:physiopathology; D010750:Phosphoproteins / Q000378:metabolism; D018336:Receptors, Aryl Hydrocarbon / Q000235:genetics* / Q000378:metabolism; D012098:Reproduction / Q000502:physiology*; D012669:Seminal Vesicles / Q000378:metabolism / Q000502:physiology*; D013739:Testosterone / Q000097:blood; D000098682:Steroidogenic Acute Regulatory Protein
chemical_list: D010750:Phosphoproteins; D018336:Receptors, Aryl Hydrocarbon; D000098682:Steroidogenic Acute Regulatory Protein; D013739:Testosterone; D015096:3-Hydroxysteroid Dehydrogenases