Insulin-Like Growth Factor I Inhibits Aromatization Induced by Follicle-Stimulating Hormone in Rat Sertoli Cell Culture1

Rappaport, Mark S.; Smith, Eric P.

doi:10.1095/biolreprod54.2.446

Cited by 25 publications

(16 citation statements)

References 52 publications

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“…Several in vitro studies have shown FSH and IGF-I take part in the regulation of Sertoli cell activity (Khan et al 2002). The effects of FSH and IGF-I when added together to cultured cells may be additive (Khan et al 2002) or antagonistic (Rappaport & Smith 1996). In the present study, deletion of the IGF-IR in Sertoli cells clearly decreased the mitotic action of FSH as well as the response of p70S6K activity to FSH (Lecureuil et al 2005).…”

Section: Discussionsupporting

confidence: 61%

Inactivation of the IGF-I receptor gene in primary Sertoli cells highlights the autocrine effects of IGF-I

Froment¹,

Vigier²,

Nègre³

et al. 2007

Journal of Endocrinology

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IGF-I regulates pituitary and gonadal functions, and is pivotal for sexual development and fertility in mammalian species. To better understand the function of autocrine IGF-I in Sertoli cell physiology, we established a system for Cre-mediated conditional inactivation of the IGF-I receptor (IGF-IR) in cultured Sertoli cells. We show here that loss of IGF-IR decreased the number of viable Sertoli cells as a consequence of diminished Sertoli cell proliferation and increased Sertoli cell death.Furthermore, the lack of IGF-IR altered the morphology of cultured Sertoli cells and decreased lactate and transferrin secretions. Collectively, our data indicate that autocrine IGF-I contributes significantly to Sertoli cell homeostasis. The described in vitro system for loss-of-function analysis of the IGF-IR can be readily transposed to study the role of other intratesticular growth factors involved in spermatogenesis.

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Section: Discussionsupporting

confidence: 61%

Inactivation of the IGF-I receptor gene in primary Sertoli cells highlights the autocrine effects of IGF-I

Froment¹,

Vigier²,

Nègre³

et al. 2007

Journal of Endocrinology

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“…When the regulation of the aromatase gene expression was analysed in terms of specific transcripts in mature rat Sertoli cells it was found that testosterone alone and follicle-stimulating hormone, either alone or with testosterone, induced an increase in the amount of P450arom mRNAs (Levallet & Carreau 1997). Whatever the somatic cells studied (either Leydig or Sertoli cells), gonadotropins provoke a dose-related increase in the P450arom mRNA levels but the nadirs are different: between 3 and 6 h in Sertoli cells (Rappaport & Smith 1996) whereas we found no changes until 6 h in Leydig cells, the maximum being observed after 24 h. Therefore LH (and cyclic AMP) controls the P450arom gene expression in the rat Leydig cells via the existence of cyclic AMP response motifs (CRE) localized in the proximal promoter PII of the aromatase gene (Bulun et al 1993). It is noteworthy that in both rat Sertoli cells (Levallet & Carreau 1997) and Leydig cells (data herein) we have been able to measure specific mRNA transcripts of aromatase without any hormonal treatment.…”

Section: Discussionmentioning

confidence: 97%

Regulation of cytochrome P450 aromatase gene expression in adult rat Leydig cells: comparison with estradiol production

Genissel¹,

Levallet²,

Carreau³

2001

Journal of Endocrinology

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Regulation of aromatase gene expression in purified rat Leydig cells has not yet been investigated. Therefore, using a highly specific quantitative RT-PCR method, we have measured the amount of cytochrome P450 aromatase (P450arom) mRNA and aromatase activity in mature rat Leydig cells submitted to various treatments during 24 h. Estradiol production was enhanced in a dose-related manner in the presence of testosterone, the maximum (28% increase) being obtained with 200 ng/ml. Related to the P450arom mRNA levels, a decrease was observed in the presence of low concentrations (50 and 100 ng/ml) of testosterone, then a 20% increase of the amount of transcripts was recorded for the higher concentrations (200-500 ng/ml). The same result was obtained in the presence of 5 -dihydrotestosterone (an androgen resistant to aromatase activity). The addition of ovine LH (oLH; 0·1-50 ng/ml) to the Leydig cell culture medium induced a dose-related augmentation of estradiol output up to 10 ng/ml oLH, although a decrease was observed with 50 ng/ml when compared with maximal values. mRNA levels slightly decreased in the presence of low concentrations (0·1-1 ng/ml) of oLH, an effect that was abolished by the addition of testosterone; mRNA levels were increased by oLH (5-10 ng/ml) 35 and 75% respectively in the absence and presence of testosterone (when compared with Leydig cells incubated without treatment). With 50 ng/ml oLH, a large augmentation (twofold) of the P450arom mRNA level either without or with testosterone was observed. Dibutyryl cyclic AMP (1 mM) mimicked the effect of oLH. The half-life of the P450arom mRNAs was twofold increased in the presence of testosterone and oLH when compared with the half-life in the absence of treatment (5·8 0·6 h). Taken together, our data have demonstrated that, in freshly isolated Leydig cells from mature rat testes, the regulation of aromatase expression and enzymatic activity is under LH (through cyclic AMP) and steroid control; moreover seminiferous tubule-secreted factor(s) are also involved. Therefore, rat Leydig cell aromatase is controlled at both transcriptional and post-transcriptional steps by endocrine and/or locally produced modulators.

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“…In addition to FSH and LH, IGF-I is thus an essential requirement for sexual development and testicular function (see [41] for a review). The mechanism of action for IGF-I effects on the reproduction system has not been fully understood but could involve regulation of the aromatization process [19], [42]. The administration of IGF-I reduced aromatase gene expression in Sertoli cells through interfering with either the production or the degradation of mRNAs [19].…”

Section: Discussionmentioning

confidence: 99%

“…The mechanism of action for IGF-I effects on the reproduction system has not been fully understood but could involve regulation of the aromatization process [19], [42]. The administration of IGF-I reduced aromatase gene expression in Sertoli cells through interfering with either the production or the degradation of mRNAs [19]. It had similar effects to FSH in terms of increasing cellular proliferation, lactate production as well as glucose and amino acid transfer [43].…”

Section: Discussionmentioning

confidence: 99%

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Synergistic Effect of Fadrozole and Insulin-Like Growth Factor-I on Female-To-Male Sex Reversal and Body Weight of Broiler Chicks

et al. 2014

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The aim of this study was to investigate the effects of Fadrozole hydrochloride and recombinant human insulin-like growth factor I (rhIGF-I) on female-to-male sex reversal, hatching traits, and body weight of broiler chickens. On the third day of incubation, fertile eggs were randomly assigned to five experimental groups comprising (i) Fadrozole (0.1 mg/egg), (ii) rhIGF-I (100 ng/egg), (iii) Fadrozole (0.1 mg/egg) + rhIGF-I (100 ng/egg), (iv) vehicle injection (10 mM acetic acid and 0.1% BSA), and (v) non-injected eggs. Eggs in the rhIGF-I-injected groups showed the mode of hatching time at the 480th hour of incubation, 12 hours earlier compared to the other groups, with no statistically significant difference in mortality and hatchability. On Day 1 and 42 of production, 90% of genetically female chicks were masculinized using Fadrozole treatment, while 100% female-to-male phenotypic sex reversal was observed in the Fadrozole+rhIGF-I group. Fadrozole equalized the body weight of both genders, although rhIGF-I was effective on the body weight of male chicks only. Interestingly, combined rhIGF-I and Fadrozole could increase the body weight in both sexes compared to the individual injections (P<0.05). These findings revealed that (i) IGF-I-treated chicken embryos were shown to be an effective option for overcoming the very long chicken deprivation period, (ii) the simultaneous treatment with Fadrozole and IGF-I could maximize the female-to-male sex reversal chance, (iii) the increase in the body weight of masculinized chickens via Fadrozole could be equal to their genetically male counterparts, and (iv) the IGF-I effectiveness, specifically along with the application of aromatase inhibitors in female chicks, indicates that estrogen synthesis could be a stumbling block for the IGF-I action mechanism in female embryos.

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Insulin-Like Growth Factor I Inhibits Aromatization Induced by Follicle-Stimulating Hormone in Rat Sertoli Cell Culture1

Cited by 25 publications

References 52 publications

Inactivation of the IGF-I receptor gene in primary Sertoli cells highlights the autocrine effects of IGF-I

Inactivation of the IGF-I receptor gene in primary Sertoli cells highlights the autocrine effects of IGF-I

Regulation of cytochrome P450 aromatase gene expression in adult rat Leydig cells: comparison with estradiol production

Synergistic Effect of Fadrozole and Insulin-Like Growth Factor-I on Female-To-Male Sex Reversal and Body Weight of Broiler Chicks

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