Evaluation of the role of FSH in regulation of Leydig cell function during different stages of its differentiation.
The role of follicle stimulating hormone (FSH) in Leydig cell function was evaluated by a passive neutralization approach at different stages of Leydig cell development. Neutralization of endogenous FSH in neonatal rats (10-day-old) resulted in reduction of testes weight, however the testicular testosterone levels and in vitro testosterone production by purified Leydig cells were elevated. Administration of FSH antiserum to immature (25-28-day-old) and adult (90-day-old) rats did not have any effect on testes weight, serum testosterone and testicular testosterone. Interestingly, there was a significant reduction in testosterone production by isolated Leydig cells under hCG stimulated and 22-R-hydroxycholesterol (22-R-OH CHOL) saturated conditions. In support of this observation administration of recombinant FSH to immature and adult rats resulted in significant increase in testosterone production by Leydig cells following incubations in presence of hCG and saturating concentrations of 22-R-OH CHOL, although there was no change in serum and testicular testosterone levels. The role of FSH in immature rats was also confirmed employing FSH receptor antiserum which was raised against the unique domains of FSH receptor. RT-PCR analysis revealed a significant reduction in the mRNA levels of StAR and IGF-1 following blockade of FSH action by FSH receptor antiserum. The results of our studies suggest a stage specific function for FSH in regulation of Leydig cell development by modulating the LH responsiveness and steroidogenesis.
Sriraman
Venkataraman
V
Department of Biochemistry, Indian Institute of Science, Bangalore 560 012, India. sriraman@bcm.tmc.edu
Jagannadha Rao
A
A
D000818:Animals; D002454:Cell Differentiation / Q000187:drug effects / Q000502:physiology; D006063:Chorionic Gonadotropin / Q000494:pharmacology; D005640:Follicle Stimulating Hormone / Q000037:antagonists & inhibitors / Q000276:immunology / Q000502:physiology*; D015870:Gene Expression; D006888:Hydroxycholesterols / Q000494:pharmacology; D007106:Immune Sera / Q000494:pharmacology; D007334:Insulin-Like Growth Factor I / Q000235:genetics; D007985:Leydig Cells / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D008297:Male; D010750:Phosphoproteins / Q000235:genetics; D051381:Rats; D011962:Receptors, FSH / Q000276:immunology; D011974:Receptors, LH / Q000235:genetics; D013254:Steroid 17-alpha-Hydroxylase / Q000235:genetics; D013737:Testis / Q000187:drug effects / Q000502:physiology; D013739:Testosterone / Q000032:analysis / Q000378:metabolism; D000098682:Steroidogenic Acute Regulatory Protein
D006063:Chorionic Gonadotropin; D006888:Hydroxycholesterols; D007106:Immune Sera; D010750:Phosphoproteins; D011962:Receptors, FSH; D011974:Receptors, LH; D000098682:Steroidogenic Acute Regulatory Protein; C003585:22-hydroxycholesterol; D013739:Testosterone; D007334:Insulin-Like Growth Factor I; D005640:Follicle Stimulating Hormone; D013254:Steroid 17-alpha-Hydroxylase