Regulation of Seminiferous Tubular Function by FSH and Androgen

Hansson, V.; Weddington, S. C.; McLean, W. S.; Smith, Albert A.; Nayfeh, Shihadeh N.; French, Frank S.; Ritzén, E. M.

doi:10.1530/jrf.0.0440363

Cited by 54 publications

(17 citation statements)

References 33 publications

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“…Calculations of the half-life for the two gonadotrophins in cattle gave nearly identical values of 35 min for LH (Schams & Karg, 1969c) and of 38 min for FSH (Schallenberger, 1977) (Hansson et al, 1975), providing a vehicle for testos¬ terone secreted from the Leydig cells under the stimulus of the LH surge.…”

Section: Methodsmentioning

confidence: 99%

Relationships between short-term variations of LH, FSH, prolactin and testosterone in peripheral plasma of prepubertal bulls

Schams¹,

Gombe²,

Schallenberger³

et al. 1978

Reproduction

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Summary. In 2 prepubertal bulls 10-min blood samples collected during a 24-h period showed that gonadotrophin and testosterone peaks occurred regularly at intervals of 6 h in one animal and 8 h in the other. There was a clear relationship between the LH, FSH and testosterone peaks. The increase of gonadotrophin levels was followed 20 \ m=+-\ 6 (s.d.) min later by an increase of testosterone; the interval between the peak values was 61\m=+-\9(s.d.) min. The pattern of prolactin concentrations differed; there were two prolonged elevations rather than regular peaks.

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Section: Methodsmentioning

confidence: 99%

Relationships between short-term variations of LH, FSH, prolactin and testosterone in peripheral plasma of prepubertal bulls

Schams¹,

Gombe²,

Schallenberger³

et al. 1978

Reproduction

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“…Testosterone alone can maintain complete spermatogenesis, but the synergistic action of FSH is necessary to normalize quantitative aspects of spermatogenesis (Steinberger 1971, Bartlett et al 1989, McLachlan et al 1996. This effect is explained by an FSH-dependent formation of the androgen-binding protein (ABP) by the Sertoli cells, which accumulate androgens in the tubuli (Hansson et al 1975, Weddington et al 1975.…”

Section: Introductionmentioning

confidence: 99%

Involvement of glucocorticoids in testicular involution after active immunization of boars against GnRH

Wagner¹,

Claus²

2004

Reproduction

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Active GnRH immunization of boars inhibits LH and testicular steroids but the consequences for spermatogenesis are unknown. Six boars were immunized three times against GnRH at 20, 24 and 28 weeks. Another six boars served as controls. Plasma LH and FSH were determined at 28 and 31 weeks. Testosterone and cortisol were determined before killing the pigs at 32 weeks. Tissue samples were taken for histology and fluid from the seminiferous tubuli for steroid determination. Individual germ cells were counted in histological sections. The glucocorticoid receptor (GCR), mitosis of spermatogonia and apoptosis were characterized by immunocytochemistry. Immunization reduced LH and testosterone to base levels whereas FSH was not changed. Testis weight was reduced by 64% due to a loss of Leydig cell cytoplasm (90.3%) and a decrease of tubule diameters (60.6%). Except for A-spermatogonia, all other spermatogenic cells were reduced by about 60%. Mitosis was reduced in immunized boars. Expression of GCRs was limited to spermatogonia and differed between immunized boars (8% of spermatogonia) and controls (2%). In the controls, androgen concentrations in tubular fluid were tenfold higher compared with immunized boars. Cortisol concentrations were of the order of 40 nmol/l both in the tubular fluid and blood plasma. These concentrations did not differ between groups. Apoptosis occurred only in spermatogonia and pachytene spermatocytes and was twofold higher in immunized boars compared with controls. Thus the availability of glucocorticoids in the tubuli and the expression of GCRs initiate apoptosis, which in turn reduces sperm yield. Testosterone is known to be an inhibitor of GCR expression, thus increasing the efficiency of spermatogenesis.

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“…FSH is thought to play a major role in the initiation of spermatogenesis in immature mammals, but is also involved in quantitative and qualitative maintenance of spermatogenesis in adult animals, in particular in primates (Clermont and Harvey, 1967;Steinberger, 1971; *Corresponding author, Fax: +3 1 10 4366832. Hansson et al, 1975a;Means et al, 1976;Marshall et al, 1986;Moudgal et al, 1992). This is supported by the observation that experimental immunization of male bonnet monkeys to ovine-FSH resulted in reversible infertility (Moudgal et al, 1992).…”

Section: Introductionmentioning

confidence: 94%

Regulation of gene expression in Sertoli cells by follicle-stimulating hormone (FSH): cloning and characterization of LRPR1, a primary response gene encoding a leucine-rich protein

Slegtenhorst-Eegdeman

Post

Baarends

et al. 1995

Molecular and Cellular Endocrinology

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Searching for hormone-regulated genes in testicular Sertoli cells, we cloned and sequenced a cDNA of 3108 base pairs, named LRPRl (signifying leucine-rich primary response gene 1). This cDNA sequence has an open reading frame of 2238 base pairs encoding a leucine-rich protein of 746 amino acid residues with a relative molecular mass of 85.6 kDa. As much as 16% of the amino acid residues is leucine. Database analysis revealed significant similarity of LRPRl to the human brain cDNA sequence ESTO0443, but not to any other sequences present in databases. The expression of LRPRI mRNA in Sertoli cells is strongly and rapidly up-regulated by follicle-stimulating hormone (FSH). The level of LRPRl mRNA was very low in Sertoli cells isolated from 21-day-old rats and cultured for 3 days in the absence of FSH, but LRPRI mRNA expression was markedly increased within 2 h after addition of FSH to these cultures. A maximal response was reached within 4 h. Dibutyryl-cyclic AMP [(Bu)+AMP] and forskolin had similar effects compared to FSH, indicating that CAMP acts as a second messenger in the regulation of LRPRl expression. The up-regulation of LRPRl mRNA expression by FSH was also observed in the presence of the protein synthesis inhibitor cycloheximide, indicating that FSH regulates LRPRI mRNA expression through a direct mechanism which does not require de novo protein synthesis. Thus, LRPRI represents a primary response gene in FSH action on Sertoli cells. The presently available data indicate that LRPRI mRNA expression is regulated specifically by FSH, since several other hormones and growth factors did not affect LRPRI mRNA expression in the cultured Sertoli cells. LRPRI mRNA expression is relatively high in testis, ovary and spleen. A much lower mRNA level was found in brain and lung, and no expression was detected in liver, kidney, heart, muscle, pituitary gland, prostate, epididymis and seminal vesicle.The basal level of testicular LRPRI expression in intact 21-day-old rats was markedly increased within several hours after a single i.p. injection of FSH, indicating that in vivo LRPRI mRNA expression may appear to be a useful parameter to evaluate testicular FSH action.

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Regulation of Seminiferous Tubular Function by FSH and Androgen

Cited by 54 publications

References 33 publications

Relationships between short-term variations of LH, FSH, prolactin and testosterone in peripheral plasma of prepubertal bulls

Relationships between short-term variations of LH, FSH, prolactin and testosterone in peripheral plasma of prepubertal bulls

Involvement of glucocorticoids in testicular involution after active immunization of boars against GnRH

Regulation of gene expression in Sertoli cells by follicle-stimulating hormone (FSH): cloning and characterization of LRPR1, a primary response gene encoding a leucine-rich protein

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