Changes in steroidogenic enzyme and steroidogenic acute regulatory protein messenger RNAs in ovarian follicles during ovarian development of rainbow trout (Oncorhynchus mykiss)

2005 ◽  
Vol 144 (3) ◽  
pp. 224-231 ◽  
Author(s):  
Ikumi Nakamura ◽  
Jennifer C. Evans ◽  
Makoto Kusakabe ◽  
Yoshitaka Nagahama ◽  
Graham Young
Keyword(s):  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Ovarian Development ◽  
Regulatory Protein ◽  
Ovarian Follicles ◽  
Steroidogenic Acute Regulatory Protein ◽  
Messenger Rnas ◽  
Steroidogenic Enzyme ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Steroidogenic Acute Regulatory

scholarly journals Changes in mRNAs encoding steroidogenic acute regulatory protein, steroidogenic enzymes and receptors for gonadotropins during spermatogenesis in rainbow trout testes

2006 ◽  
Vol 189 (3) ◽  
pp. 541-554 ◽  
Author(s):  
M Kusakabe ◽  
I Nakamura ◽  
J Evans ◽  
P Swanson ◽  
G Young
Keyword(s):  
Cytochrome P450 ◽  
Rainbow Trout ◽  
Reproductive Cycle ◽  
Regulatory Protein ◽  
Hydroxysteroid Dehydrogenase ◽  
Steroidogenic Acute Regulatory Protein ◽  
Fsh Receptor ◽  
Steroidogenic Enzyme ◽  
Lh Receptor ◽  
Steroidogenic Acute Regulatory

In vertebrates, sperm development and maturation are directly regulated by gonadal steroid hormone secretion. The relationships among the expression of genes encoding steroidogenic proteins and receptors for gonadotropins, and testicular steroid production have not yet been comprehensively determined in male teleosts. In this study, the changes in levels of mRNAs encoding follicle-stimulating hormone (FSH) receptor, luteinizing hormone (LH) receptor, steroidogenic acute regulatory protein (StAR), cytochrome P450 cholesterol side-chain cleavage, 3β-hydroxysteroid dehydrogenase/Δ5–4-isomerase, cytochrome P450 17α-hydroxylase/17,20-lyase, cytochrome P450 11β-hydroxylase, 11β-hydroxysteroid dehydrogenase and 20β-hydroxysteroid dehydrogenase were determined by real-time, quantitative PCR assays and related to changes in serum steroid levels throughout the reproductive cycle in male rainbow trout. Serum 11-ketotestosterone and 17α,20β-dihydroxy-4-pregnen-3-one levels were measured by RIA. Although the pattern of change in the mRNA levels for the enzymes was variable, the increases in steroidogenic enzyme mRNAs started prior to a significant increase of serum steroid levels. The patterns of transcript levels of FSH and LH receptors suggest that changes in StAR and steroidogenic enzyme transcripts are largely mediated by the FSH receptor during early and mid-spermatogenesis and by the LH receptor during late spermatogenesis and spermiation. Levels of StAR (10-fold) and P450 17α-hydroxylase/17,20-lyase (sevenfold) transcripts changed with the greatest magnitude and were closely related to the changes in serum steroids, suggesting that changes in StAR and P450 17α-hydroxylase/17,20-lyase abundance are likely to be the major influences on overall steroidogenic output during the reproductive cycle in male rainbow trout.

scholarly journals Luteinizing Hormone/Human Chorionic Gonadotropin-Mediated Activation of mTORC1 Signaling Is Required for Androgen Synthesis by Theca-Interstitial Cells

2012 ◽  
Vol 26 (10) ◽  
pp. 1732-1742 ◽  
Author(s):  
Murugesan Palaniappan ◽  
K. M. J. Menon
Keyword(s):  
Chorionic Gonadotropin ◽  
Regulatory Protein ◽  
Steroidogenic Acute Regulatory Protein ◽  
Steroidogenic Enzymes ◽  
Steroidogenic Enzyme ◽  
S6 Kinase ◽  
Ribosomal Protein S6 ◽  
Mtorc1 Signaling ◽  
Steroidogenic Acute Regulatory ◽  
I Cells

Abstract LH triggers the biosynthesis of androgens in the theca-interstitial (T-I) cells of ovary through the activation of a cAMP-dependent pathway. We have previously shown that LH/human chorionic gonadotropin (hCG) activates mammalian target of rapamycin complex 1 (mTORC1) signaling network, leading to cell proliferation. In the present study, we provide evidence that the LH/hCG-mediated activation of the mTORC1 signaling cascade is involved in the regulation of steroidogenic enzymes in androgen biosynthesis. Treatment with LH/hCG increased the expression of downstream targets of mTORC1, ribosomal protein S6 kinase 1, and eukaryotic initiation factor 4E as well as steroidogenic enzymes. LH/hCG-mediated stimulation of the steroidogenic enzyme mRNA was blocked by the mTORC1 inhibitor, rapamycin. This inhibitory effect was selective because rapamycin failed to block hCG-mediated increase in the expression of Star mRNA levels. Furthermore, pharmacological targeting of mTORC1 with rapamycin also blocked LH/hCG- or forskolin-induced expression of cAMP response element-binding protein (CREB) and steroidogenic enzymes (P450 side-chain cleavage enzyme, 3β-hydroxysteroid dehydrogenase type 1, and 17α-hydroxylase/17,20 lyase) but produced no effect on steroidogenic acute regulatory protein levels. These results were further confirmed by demonstrating that the knockdown of mTOR using small interfering RNA selectively abrogated the LH/hCG-induced increase in steroidogenic enzyme expression, without affecting steroidogenic acute regulatory protein expression. LH/hCG-stimulated androgen production was also blocked by rapamycin. Furthermore, the pharmacological inhibition of mTORC1 or ribosomal protein S6 kinase 1 signaling prevented the LH/hCG-induced phosphorylation of CREB. Chromatin immunoprecipitation assays revealed the association of CREB with the proximal promoter of the Cyp17a1 gene in response to hCG, and this association was reduced by rapamycin treatment. Taken together, our findings show for the first time that LH/hCG-mediated activation of androgen biosynthesis is regulated by the mTORC1 signaling pathway in T-I cells.

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