Abstract
The roles of FSH and androgen in the postnatal development of Sertoli cell number and function have been investigated using mice that lack FSH (FSHbetaKO), FSH-receptors (FSHRKO), or androgen receptors (Tfm). At birth and d 5, Sertoli cell number was normal in FSHRKO and FSHbetaKO mice, but was significantly reduced on d 20 and in adulthood. In contrast, Sertoli cell number was reduced at birth in Tfm mice and remained significantly less than normal up to adulthood. Sertoli cell activity was determined through measurement of 11 different mRNA transcript levels. From birth to adulthood, the expression of most transcripts increased, with a significant rise occurring between d 5 and 10. In animals lacking FSH stimulation, mRNA expression (measured per Sertoli cell) was largely normal on d 5, but was reduced in seven transcripts on d 20 and in five transcripts at adulthood. In Tfm mice two transcripts showed reduced expression on d 5, and four were reduced on d 20, although expression in adult Tfm mice did not differ from that in normal cryptorchid controls. The results show that 1) testosterone, but not FSH, is required for Sertoli cell proliferation during fetal and early neonatal life; 2) FSH and testosterone both regulate the late stages of Sertoli cell proliferation; 3) FSH has a general trophic effect on Sertoli cell activity in the pubertal and adult mouse; and 4) androgens are required for specific transcript expression during prepubertal development. Specific effects of androgens were not seen in the adult, although these may be masked by the effects of cryptorchidism.
Original language | English |
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Pages (from-to) | 318-29 |
Number of pages | 12 |
Journal | Endocrinology |
Volume | 145 |
Issue number | 1 |
DOIs | |
Publication status | Published - 1 Jan 2004 |
Keywords
- androgens/metabolism
- animals
- female
- follicle stimulating hormone, beta subunit/genetics
- gene expression regulation, Developmental
- male
- mice
- mice, inbred C57BL
- mice, mutant Strains
- RNA, messenger/analysis
- receptors, androgen/genetics
- receptors, FSH/genetics
- Sertoli cells/cytology
- testis/cytology