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At least 433 records · Page 24Linked to original sources
PubMed2000

Development of a long-term serum-free culture system for immature granulosa cells from diethylstilboestrol-treated prepubertal rabbits: influence of androstenedione and fibronectin on FSH-induced cytodifferentiation.

Granulosa cells from diethylstilboestrol-treated prepubertal rabbits were cultured for 6 days in M199 with FSH (1-100 ng ml(-1)) in uncoated or fibronectin-coated plates with or without androstenedione to define the time course profile of oestradiol and progesterone secretion, and the possible modulator role of androstenedione and fibronectin during FSH-induced rabbit granulosa cell differentiation. Every 48 h, cultures were photographed and samples of medium were collected and assayed by ELISA for oestradiol and progesterone. FSH increased oestradiol secretion in a dose-dependent manner. Androstenedione augmented FSH-stimulated oestradiol secretion, and led to a decrease in secretion of oestradiol with time in culture. FSH stimulated progesterone secretion in a dose-dependent manner. This was increased by androstenedione with 10 ng FSH ml(-1) (0-96 h) and 1 ng FSH ml(-1) (96-144 h). FSH-stimulated (100 ng ml(-1)) progesterone secretion decreased at 48-96 h. Fibronectin prevented this decrease, without affecting oestradiol or progesterone secretion at other time points. FSH caused cell reaggregation at 48 h. In conclusion, this serum-free culture system is appropriate for the study of mechanisms of rabbit granulosa cell differentiation. FSH induced cytodifferentiation and reaggregation of granulosa cells. Androstenedione appeared to act synergistically with FSH to promote steroidogenesis. Fibronectin sustained progesterone secretion during differentiation.

Androstenedione↗
PubMed1989

Differential effects of FSH and testosterone on the maintenance of spermatogenesis in the adult hypophysectomized rat.

In order to clarify further the role of FSH in the maintenance of spermatogenesis, adult rats were treated with purified human FSH (2 X 5 IU/day per rat), testosterone (1.5 cm silicone elastomer implant) or a combination of both hormones for 2 weeks following hypophysectomy. After hypophysectomy alone, no elongate spermatids were observed and the numbers of pachytene spermatocytes and round spermatids observed were reduced when compared with untreated controls. Testosterone supplementation alone qualitatively maintained the formation of elongate spermatids in most seminiferous tubules, whilst in FSH-treated rats increased numbers of round spermatids and pachytene spermatocytes were observed when compared with hypophysectomized animals. Formation of elongate spermatids, however, did not occur under FSH treatment alone. A combination of FSH and testosterone treatment maintained spermatogenesis in an almost quantitative fashion. Numbers of pachytene spermatocytes and round spermatids were maintained at about 80% of levels seen in intact control animals. Treatment with FSH or testosterone alone maintained testis weights at significantly higher levels than those seen in hypophysectomized controls (FSH, 0.79 +/- 0.05 g; testosterone, 0.81 +/- 0.07 g; hypophysectomized, 0.50 +/- 0.04 g). Animals treated with FSH and testosterone showed testis weights 20% below control values (1.22 +/- 0.05 vs 1.51 +/- 0.06 g; P less than 0.05). No increases in intratesticular or intratubular androgen concentrations or in testosterone: dihydrotestosterone ratios were observed in any of the hormone-treated groups when compared with hypophysectomized controls. In all hypophysectomized animals testicular androgen concentrations were reduced to less than 5% of control values. The results obtained in this study suggest that FSH is involved in the maintenance of spermatogenesis in the adult rat and that the effects of FSH are not mediated through changes in intratesticular androgens. Low levels of testosterone in combination with FSH can almost quantitatively maintain spermatogenesis in adult rats.

Androgens↗
PubMed1992

Antiprogesterone RU486 induces dissociation of LH and FSH secretion in the cyclic rat: effect of anti-inhibin serum.

Administration of the antiprogesterone RU486 to 4-day cyclic rats from metoestrus to pro-oestrus increases serum levels of LH while decreasing levels of FSH. If it is assumed that there is only one gonadotrophin-releasing hormone, there is no direct explanation for the decrease in FSH concentrations. The purpose of these experiments was to investigate the effect of RU486 on gonadotrophin secretion in cyclic rats during periods when the secretion of LH and FSH diverges. RU486 blunted the transient increase in FSH concentration on the afternoon of metoestrus and the compensatory ovarian hypertrophy on the next day of oestrus in unilaterally ovariectomized 4-day cyclic rats. In addition, bilateral ovariectomy reversed the effect of RU486 on the basal secretion of FSH. RU486 induced an increase in basal LH concentrations. Since ovarian inhibin decreases the basal release of FSH, and decreases in peripheral inhibin seem to be responsible for the transient rise in FSH during the oestrus cycle, the effect of RU486 on serum levels of LH and FSH during dioestrus in rats injected with a sheep anti-inhibin serum (AIS) were further evaluated. Treatment with AIS increased FSH levels in oil-treated rats without altering the levels of LH. In contrast, the effects of AIS on FSH secretion were blunted in RU486-treated rats. The results suggest that inhibin might be involved in the RU486-induced decrease of FSH secretion in cyclic rats.

Animals↗
PubMed2005

Lindane, a gap junction blocker, suppresses FSH and transforming growth factor beta1-induced connexin43 gap junction formation and steroidogenesis in rat granulosa cells.

The present study was designed to explore the role of gap junctions in follicle-stimulating hormone (FSH) and transforming growth factor beta1 (TGF beta1)-stimulated steroidogenesis in ovarian granulosa cells of gonadotropin-primed immature rats. There were three specific aims. First, we investigated the effect of FSH and TGF beta1 as well as lindane (a general gap junction blocker) on the level of connexin43 (Cx43), the major gap junction constituent in granulosa cells, and on gap junction function. The second aim was to determine the effect of lindane on FSH and TGF beta1-stimulated progesterone production and the levels of two critical players, cytochrome P450 side-chain cleavage (P450scc) enzyme and steroidogenic acute regulatory (StAR) protein. The third aim was to further investigate the specific involvement of Cx43 gap junctions in FSH and TGF beta1-stimulated steroidogenesis using a Cx43 mimetic peptide blocker. Immunoblotting analysis showed that FSH plus TGF beta1 dramatically increased the levels of phosphorylated Cx43 without significantly influencing the level of nonphosphorylated Cx43, and this stimulatory effect was completely suppressed by lindane. Also, immunofluorescence analysis showed that Cx43 immuno-reactivity increased in the FSH plus TGF beta1-treated group and predominantly appeared in a punctate pattern at cell-cell contact sites, and lindane reduced such cell periphery immunostaining. Furthermore, TGF beta1 enhanced the FSH-induced gap junction intercellular communication and lindane completely suppressed this effect. In addition, lindane suppressed the FSH and TGF beta1-stimulated increases in progesterone production and the levels of P450scc enzyme and StAR protein. This study demonstrates a clear temporal association between the Cx43 protein level/gap junction communication and progesterone production in rat ovarian granulosa cells in response to FSH and TGF beta1 as well as lindane. Furthermore, a specific Cx43 gap junction blocker suppressed FSH plus TGF beta1-stimulated progesterone production. In conclusion, this study suggests that Cx43 gap junctions may play a critical role in FSH plus TGF beta1-stimulated progesterone production in rat ovarian granulosa cells.

Animals↗
PubMed1991

Prepubertal changes in plasma FSH and inhibin in Holstein bull calves: responses to castration and(or) estradiol.

The objectives of two studies were to determine 1) whether plasma concentrations of inhibin (INH) changed with age in prepubertal bulls and whether these changes were related to changes in FSH, testosterone or testis length; and 2) whether castration and(or) estradiol implants affected plasma concentrations of INH and FSH. In Exp. 1, plasma INH remained constant from 4 until 8 wk of age then increased from 120 pM to 202 pM between 8 and 12 wk. Thereafter, INH decreased to 90 pM by 36 wk. Between 4 and 10 wk, plasma FSH increased from .32 to .43 ng/ml, apparently increasing before the initial rise in plasma INH. Between 10 and 12 wk, FSH declined from .43 to .33 ng/ml. After 12 wk, FSH increased as INH decreased. Initial increases in testis length and concentrations of plasma testosterone occurred at 14 wk coincident with the second rise in FSH. In Exp. 2, bull calves were either left intact, castrated, castrated and implanted with estradiol, or left intact and implanted with estradiol at 7.5 wk of age. Castration decreased concentrations of INH and increased concentrations of FSH. Castrated calves implanted with estradiol had decreased concentrations of both INH and FSH. Intact bulls implanted with estradiol had decreased concentrations of FSH relative to intact unimplanted bulls; however, concentrations of INH did not display the age-related changes observed in intact, unimplanted bulls. In summary, age-related changes in plasma INH and FSH occur in bulls. Furthermore, plasma concentrations of INH and FSH increased before changes in gonadal size were detected. The bovine testis may be a major source of circulating INH because castration decreased concentrations of plasma INH.

Aging↗
PubMedDate not supplied

Differential effects of FSH on the activities of S-adenosyl-L-methionine decarboxylase and ornithine decarboxylase in Rat sertoli cells.

Follicle stimulating hormone (FSH) modulates testicular function via Sertoli cells. The effect of FSH on S-adenosyl-L-methionine decarboxylase (AdoMetDC) activity was investigated in cultured Sertoli cells isolated from 18-day-old rats. In contrast to our previous finding that FSH inhibited Sertoli cell ornithine decarboxylase (ODC) activity, FSH stimulated AdoMetDC activity 160 to 300% above the level of the control cells during the initial 2 to 6 hours of treatment. The stimulated enzyme activity declined to 20 to 30% below the control values by 12 hours of exposure to FSH, and then rebounded to 120 to 125% of control values. To determine whether or not the initial opposite effects of FSH on AdoMetDC and on ODC activities are mediated by the same mechanism, various agents which increase intracellular cAMP level were used. All agents studied stimulated Sertoli cell AdoMetDC activity at 5 hours after their inclusion while they significantly inhibited ODC activity. In the presence of FSH, the stimulatory effect of these agents on AdoMetDC was either equal to or slightly greater than that caused by FSH or either agent alone. The combination of dbcGMP with FSH or with dbcAMP resulted in a synergistic or additive effect on AdoMetDC, as well as ODC, activity. The data suggest that the action of FSH on AdoMetDC activity in Sertoli cells is also mediated through cAMP, as concluded previously for ODC activity. Regardless of the effects of FSH on both enzymes, ODC always exhibited a relatively greater activity than did AdoMetDC in cultured rat Sertoli cells.

Adenosylmethionine Decarboxylase↗
PubMed1988

Oocyte maturation is regulated by modulation of the action of FSH in cumulus cells.

A biochemical and cellular model is described for the regulation of oocyte maturation by modulation of FSH-dependent accumulation of cyclic AMP (cAMP) in the rat oocyte-cumulus complex (OCC). We propose that accumulation of cAMP in cumulus cells is specifically stimulated by FSH and modulation of this response to FSH is a primary site for the control of oocyte maturation. On the one hand, adenosine amplifies inhibition of oocyte maturation by up-modulation of FSH-sensitive accumulation of cAMP. In contrast, calcium ionophores induce oocyte maturation by down-modulation of FSH-dependent accumulation of cAMP. We suggest that adenosine and calcium interact at a similar site because adenosine reverses the calcium-dependent inhibition of the action of FSH. This model appears to have physiological relevance since induction of oocyte maturation by gonadotropin in the intact follicle occurs in parallel with inhibition of the FSH-sensitive accumulation of cAMP in the OCC. Moreover, gonadotropin-induced desensitization of the OCC to the action of FSH appears to precede the loss of intercellular junctional processes, as measured indirectly by uptake of radiolabelled uridine into the oocyte. Thus, a decrease in the FSH-sensitive accumulation of cAMP in cumulus cells, produced either by direct elevation of the intracellular concentration of calcium or by treatment of the intact follicle with gonadotropin, results in oocyte maturation. On the other hand, an increase in the cAMP response to FSH, produced by agents such as adenosine, results in inhibition of oocyte maturation. Thus, responsiveness of the cumulus cells to FSH appears to be acutely modulated and this site may be a major determinant for the regulation of oocyte maturation.

Adenosine↗
PubMedDate not supplied

Hormonal regulation of spermatogenesis in the hypophysectomized rat: FSH maintenance of cellular viability during pubertal spermatogenesis.

The potential for follicle-stimulating hormone (FSH) to promote germ-cell survival and the cellular sites of FSH action were studied using a gonadally maturing (pubertal), hypophysectomized (Hx) rat model in which residual testosterone (T) activity was blocked by injections of an androgen-receptor antagonist, flutamide. Recombinant human FSH was given to androgen-deprived and androgen-blocked male rats at 27 days of age to determine maintenance of individual germ-cell types at 35 days of age. Follicle-stimulating hormone significantly increased testis weights and tubular diameters as compared with Hx and Hx-flutamide controls, although testis weights in FSH-treated animals were significantly lower than in pituitary-intact animals. Morphometric assays to determine ratios of germ cells to Sertoli cells and to determine the number of germ cells present per hour of development showed that the population of type A spermatogonia in the early stages of the cycle was not responsive to FSH. Follicle-stimulating hormone had a marked ability to maintain cell viability in the rapid, successive divisions that begin in the latter part of the cycle and that continue through the next cycle (i.e., from type A1 to A4 and from intermediate spermatogonia to type B spermatogonia to preleptotene spermatocytes to leptotene/zygotene spermatocytes to young pachytene spermatocytes). The data also suggest T responsiveness of these cell types since the Hx-FSH-flutamide group showed lower cell viability at the aforementioned steps when compared with the Hx-FSH group. Too few cell types were present at subsequent phases of spermatogenesis to allow a sensitive determination of FSH activity in the maintenance of cell viability. The data show the potential of FSH in the absence or relative absence of T activity to maintain cell viability. These data support the concept of overlapping and synergistic (or additive) effects of T and FSH in the immature rat and identify the cellular sites of FSH action.

Androgen Antagonists↗
PubMed2002

Relationship between adenylate cyclase sensitivity to follitropin and FSH receptor mRNA expression in the ovary of the lizard Podarcis sicula.

In mammals, gonadal functions are regulated by two pituitary gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), that interact with gonadal membrane receptors to activate adenylate cyclase. In comparison to mammalian systems, in squamate reptiles a reduced amount of information exists on gonadotropins and their related receptors. This study is aimed at clarifying if, in the lizard Podarcis sicula, the ovarian sensitivity to FSH is correlated to the reproductive cycle and to the expression of membrane receptors involved in the hormone recognition. The results demonstrate that the ovarian adenylate cyclase responsiveness to FSH parallels ovarian functions, being maximal during the ovulatory period. The ovarian sensitivity to FSH is also related to oocyte growth and vitellogenesis. Northern blot analyses reveal that the FSH receptor mRNA is maximally expressed in vitellogenic oocytes during the reproductive period. These results suggest that, in lizard ovary, hormone activation of adenylate cyclase is mediated by de novo synthesis of receptors specifically involved in FSH recognition. In lizards treated in vivo with FSH during the pre-ovulatory period, adenylate cyclase becomes refractory to further FSH stimulation 2 hr after treatment, but sensitivity to the hormone is restored after 2 weeks. Nevertheless, while the restored level of activity never exceeds that observed during the nonreproductive period, the expression level of FSH receptor mRNAs is significantly enhanced in these animals. These results suggest that in lizard the processes that regulate ovarian growth, vitellogenesis, and ovulation are controlled by a complex network of signals including gonadotropin, FSH receptor expression, and adenylate cyclase.

Adenylyl Cyclases↗
PubMed2004

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.

Animals↗
PubMed2006

FSH and folliculogenesis: from physiology to ovarian stimulation.

FSH is a glycoprotein hormone consisting of two peptide subunits. The role of FSH in folliculogenesis is well known: to stimulate the formation of a large pre-ovulatory follicle that, because of its FSH-dependent maturation, is capable of ovulation and forming a corpus luteum in response to the mid-cycle surge of LH. FSH is widely used in ovarian stimulation for assisted reproduction techniques. Ovarian stimulation protocols combine the use of human menopausal gonadotrophin, urinary FSH or recombinant FSH with gonadotrophin-releasing hormone (GnRH) agonists or antagonists in order to increase oocyte number and to avoid premature LH surge. Recently, the availability of recombinant LH has permitted new stimulation protocols, combining recombinant FSH, recombinant LH and GnRH antagonists. Due to the limitations of the new Italian law in terms of the number of oocytes that can be fertilized, protocols with a softer ovarian stimulation are now considered, reducing risk of ovarian hyperstimulation syndrome, multiple pregnancies and emotional and physical burdens on the patients. Long-acting FSH preparations are also under clinical study. Knowledge of the stereochemical three-dimensional structure of FSH and its receptor will allow the study of new non-peptide orally administered molecules that fit the FSH receptors.

Female↗
PubMedDate not supplied

Effect of FSH and its different isoforms on maturation of oocytes from pre-ovulatory follicles.

FSH exists as a family of isohormones exhibiting distinct oligosaccharide structures, and the released FSH isoform mixtures change during the follicular phase of the menstrual cycle. In addition, the pulsatile release of gonadotrophins seems to expose follicles to bursts of more less-acidic FSH isoforms and the follicle is likely to be exposed to an almost ever changing composition of FSH isoforms. The different isoforms causes a number of different and divergent biological effects. FSH promotes oocyte maturation, and 5-10 IU/l of less-acidic FSH isoforms are sufficient to induce oocyte maturation in vitro. Exposure of cumulus-oocyte complexes to less-acidic FSH isoforms in a pulse-like fashion results in a rapid pattern of cAMP accumulation exceeding that seen with acidic isoforms, which appear to sustain lower but more constant cAMP production. The presence of particularly less-acidic isoforms for a period exceeding 30 min causes an attenuated cAMP response. In conclusion, it appears that pulsatile and intermittent release of less-acidic/short-living FSH isoforms is sufficient to induce biological responses, while allowing the granulosa cells to regain responsiveness to further FSH stimulation. Together with the interpulse release of more acidic isoforms, overall FSH secretion seems to ensure proper follicular maturation resulting in the release of developmentally competent oocytes.

Animals↗
PubMedDate not supplied

Isoforms and single nucleotide polymorphisms of the FSH receptor gene: implications for human reproduction.

The FSH receptor shows three single nucleotide polymorphisms (SNPs), one in the promoter and two in exon 10. In addition, the FSH receptor mRNA undergoes extensive alternative splicing. While no physiological role for the SNP in the promoter and for alternative spliced isoforms has been demonstrated so far, the SNPs in exon 10 result in four discrete allelic variants characterized by the amino acid combinations Thr307-Asn680, Ala307-Ser680, Ala307-Asn680 and Thr307-Ser680. Several studies have demonstrated that the first two allelic variants are very frequent (approximately 60 and 40% respectively) in the Caucasian population. The rarer Ala307-Asn680 and Thr307-Ser680 variants are much less frequent (<5%) in the Chinese. In males the FSH receptor variants are not related to testicular volume, serum FSH or serum inhibin B levels. The two most common receptor variants transiently transfected in COS-7 cells displayed similar functional characteristics. Frequency distribution of the two polymorphisms in normal women and patients with polycystic ovarian syndrome or premature ovarian failure is still under investigation. The homozygous Ala307-Ser680 variant seems to be associated with significantly higher basal serum FSH levels and with a higher amount of FSH required for ovarian stimulation in women undergoing assisted reproduction. This suggests that the FSH receptor genotype can influence the ovarian response to FSH stimulation. The presence of SNPs in the FSH receptor gene capable of modifying FSH action paves the way for future patient-tailored, genotype-based hormone therapies.

Alleles↗
PubMed1998

Characterization and hormonal regulation of a rat ovarian insulin-like growth factor binding protein-5 endopeptidase: an FSH-inducible granulosa cell-derived metalloprotease.

Previous studies established the existence of an FSH-inducible rat granulosa cell-derived insulin-like growth factor binding protein (IGFBP)-5 endopeptidase. It was the objective of this communication to characterize this activity in some detail. Exposure of [125I]rhIGFBP-5 substrate to media conditioned by FSH-treated granulosa cells (a cell-free assay) produced two rhIGFBP-5 cleavage products (estimated size 19.5 and 17.5 kDa). The acquisition of IGFBP-5 endopeptidase activity in culture proved FSH (or PMSG) to be dose and time dependent. The addition of oFSH or rhFSH to the cell-free assay in turn, proved without effect on IGFBP-5 endopeptidase activity, thereby arguing against the possibility of an FSH receptor-independent phenomenon or of contaminating pituitary-derived contribution. The ability of FSH to induce IGFBP-5 endopeptidase activity proved relatively specific in that other granulosa cell agonists such as activin-A, IGF-I, GnRH, interleukin-1beta, TNF alpha, TGF beta1, EGF, or endothelin-1 failed to do so. However, the concurrent provision of GnRH, TNF alpha, EGF, or endothelin-1 proved inhibitory to the IGFBP-5 endopeptidase-inducing property of FSH. Activin-A and TGF beta1 in turn further stimulated the FSH effect. Sensitivity to EDTA, 1,10 phenanthroline, and high concentrations (> or = 0.1 mM) of Zn2+ suggested a Zn2+ metalloprotease. Insensitivity to TIMP-1 and TIMP-2 argued against a matrix metalloprotease (MMP). Relative insensitivity to PMSF, AMPSF, aprotinin, TPCK, and benzamidine argued against the possibility of a serine protease. Insensitivity to pepstatin A and E64 argued against aspartic and cysteine proteases, respectively. Insensitivity to plasminogen activator inhibitor-1 (PAI-1) and the presumed lack of free plasminogen in serum-free culture media argued against plasmin. Proteolysis was completely inhibited over the acid pH range but proceeded unencumbered at neutral and basic pH. Competition studies using unlabeled IGFBPs (1-6) as well as cell-free proteolysis assays of [125I]-labeled IGFBP-1, 2, 3, and 6 suggested a significant level of specificity for the FSH-induced/IGFBP-5-directed endopeptidase. Centricon-mediated fractionation of FSH-conditioned media revealed the IGFBP-5 endopeptidase activity in the fraction representing proteins of molecular weight >100K. Taken together, these observations document a secreted, granulosa cell-derived, high molecular weight, FSH-inducible, IGFBP-5-selective, neutral/basic pH-favoring, non-MMP Zn2+ metalloprotease.

Amino Acid Sequence↗
PubMed1983

Multiple species of FSH are present within hamster anterior pituitary cells cultured in vitro.

Anterior pituitary cells were obtained from ovariectomized hamsters and cultured for 4 days. The cells were lysed and intracellular proteins, including FSH, were separated by polyacrylamide gel isoelectric focusing. FSH present within cell lysates so separated was quantitated by a specific FSH radioimmunoassay (RIA). Six distinct species of intracellular FSH were observed with pI values = 5.9, 5.7, 5.3, 5.1, 4.7 and 4.3 -- 3.8. All six species were detectable when proteins from a concentrate of incubation medium collected from those cell cultures were separated by isoelectric focusing. Similar isoelectric points were obtained when the FSH species present within an anterior pituitary homogenate obtained from ovariectomized hamsters were separated by the same technique. All but two of these six species of intracellular FSH were well recognized by a hamster FSH receptor preparation. However, these two species of FSH (pI values = 4.7 and 4.3 -- 3.8) do not appear to be beta subunits of the intact glycoprotein as determined by gel filtration. Thus, the present studies demonstrate that, as observed previously in anterior pituitary glands obtained from intact and castrated animals, pituitary cells that have been enzymatically dissociated and cultured in vitro for 4 days contain and secrete multiple species of FSH that are separable by polyacrylamide gel isoelectric focusing. This in vitro system may be useful for studying the hormonal factors that regulate FSH species synthesis and secretion.

Animals↗
PubMed1990

Endorphin suppresses FSH-stimulated proliferation of isolated neonatal Sertoli cells by a pertussis toxin-sensitive mechanism.

During perinatal development, when the size of the Sertoli cell population is determined, Leydig cells produce beta-endorphin, a peptide which may interact with Sertoli cells to modify their FSH-responsiveness, as suggested by our previous work. The goal of the present study was first, to test directly the possibility that beta-endorphin modifies the proliferative response of neonatal Sertoli cells to FSH, and second, to gain information on a mechanism(s) involved in any observed effect. We treated isolated 6-day-old Sertoli cells with FSH or vehicle in vitro and measured their incorporation of exogenous, radiolabeled thymidine with quantitative autoradiography. After 2 days in culture with FSH, we detected a 10-fold increase in the rate of Sertoli cell proliferation. The level of cell division in these FSH-treated cultures was identical to that in other cultures exposed to cAMP under similar conditions. In addition, inclusion of beta-endorphin 3 hr prior to FSH or cAMP decreased the effect of the hormone by 50% but left the cAMP response unchanged. Thus, beta-endorphin acts on isolated, neonatal Sertoli cells at a point prior to intracellular production of cAMP to suppress their response to FSH. When other cultures were treated with pertussis toxin, a blocker of intracellular GTP-binding proteins such as Gi, before sequential addition of endorphin and FSH, the effect of beta-endorphin on FSH-responsiveness was abolished. Moreover, when other cultures were exposed to pertussis toxin in the absence of endorphin, followed by FSH, their response to the hormone was unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Immunohistochemical demonstration of FSH and LH in the pituitary of the developing frog, Rana esculenta.

The ontogenetic pattern of immunohistochemically detectable FSH beta and LH beta cells was investigated in the pars distalis of the pituitary of the frog, Rana esculenta. The appearance, distribution, and percentage of these cells were examined in tadpoles from soon after hatching to the end of metamorphosis and in juveniles. We used monoclonal antibodies against bullfrog FSH beta and LH beta for single staining, and either mouse anti-bullfrog LH beta + guinea pig anti-rat FSH beta or rabbit polyclonal anti-bullfrog LH beta + mouse monoclonal anti-bullfrog FSH beta for double staining. The first appearance of gonadotropes, immunopositive for FSH beta, was revealed in stage 26 tadpoles. In successive stages of development the percentage of FSH beta-positive cells increased progressively and significantly. The mean percentage of these in the pars distalis cells increased from 0.7% in stage 26 to nearly 10% during the metamorphic climax (stages 31-33). In juveniles, the mean percentage of FSH beta-positive cells increased more than twofold compared to the climax value. The appearance of LH beta-positive cells was first recorded during the climax, and the mean percentage of LH beta-positive cells in juveniles reached levels as high as 30% or more, exceeding the number of FSH beta-positive cells. In climax, all LH beta-positive cells stained with anti-FSH beta as well. In juveniles, however, up to 80% of gonadotropes demonstrated colocalization of FSH beta and LH beta staining. We argue that both gonadotropins may be synthesized in all gonadotropes, and a small number of cells immunoreactive to either of the two gonadotropins may simply indicate that at that particular moment the cell contained detectable amounts of only one form of gonadotropin. These observations are discussed in relation to the possible involvement of hypothalamic influence in the differentiation of gonadotropes of the pituitary.

Animals↗
PubMed1977

Effect of follicle-stimulating hormone (FSH) and estrogen on follicle growth in rats.

The effect of follicle-stimulating hormone (FSH) and diethylstilbestrol (DES) on ovarian follicle growth was studied in hypophysectomized rats, using histologic, autoradiographic and histochemical techniques. The administration of FSH to immature hypophysectomized rats stimulated the follicle growth with thickening of the theca layer and repair of "deficiency cells". Although DES given to hypophysectomized rats also stimulated the follicle growth, the theca layer was relatively thin compared with that in FSH-treated rats. In order to detect cell division in a growing follicle, the number of labelled granulosa cells with tritiated thymidine as a proportion of the granulosa cells in a growing follicle were counted and the labelling indices of the granulosa cells were calculated. The labelling indices increased by the administration of FSH (p less than 0.05) or DES (p less than 0.05). The uptake of tritiated thymidine and leucine by the theca cells was enhanced only by FSH and was not stimulated by DES. The administration of FSH resulted in an increase of the histochemically demonstrable enzyme activity such as delta5-3beta-hydroxysteroid dehydrogenase (3beta-HSD) or alkaline phosphatase in the theca cells. In contrast, the administration of DES did not stimulate the enzyme activity of the theca cells. Furthermore, FSH stimulated a release of estradiol and estriol from the ovary of hypophysectomized rat, whereas DES did not. Although ovarian follicle growth was stimulated by both FSH and DES, the effect of the two hormones on the theca cells was quite different and the secretion of estrogen was stimulated by FSH. The results suggest that FSH induced follicle growth of the ovary might be mediated by estrogen produced by the theca cells.

Alkaline Phosphatase↗