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PubMed2003

Gonadotropin (LH, FSH) levels in serum and cyst fluid in epithelial tumors of the ovary.

OBJECTIVES: The aim of this work was to determine gonadotropin (LH, FSH) levels in serum and cyst fluid in various type of ovarian epithelial neoplasms (benign, borderline, malignant) and to compare them with levels in benign cysts. Additionally we decided to estimate if there were some significant correlations between serum and ovarian cyst fluid in gonadotropin levels in all investigated groups. MATERIALS AND METHODS: The study group included 74 patients before (n=36) and after (n=38) menopause, divided into four groups depending on the histopathologic diagnosis. Serum and cyst fluid levels of LH and FSH were determined in all patients. RESULTS: We found statistically significant differences concerning LH and FSH levels in serum and cyst fluid between malignant and borderline tumors, between malignant tumors and benign cystadenomas and between malignant tumors and non-neoplastic cysts. We also found statistically significant correlations between serum and cyst fluid as to FSH and LH levels in patients with borderline tumors. There were no statistically significant correlations between serum and cyst fluid as to FSH and LH levels in patients with malignant epithelial tumors (group 1) and in patients with benign cystadenomas (group 3). CONCLUSIONS: High FSH and LH levels in cyst fluid of malignant epithelial tumors of the ovary are in line with the gonadotropin theory of tumor growth. Simultaneous determination of various types inhibin levels appears to be an interesting topic for our future research.

Adenocarcinoma, Mucinous↗
PubMed1985

FSH regulates cultured Leydig cell function via Sertoli cell proteins: an in vitro study.

The effects of follicular stimulating hormone (FSH) on testicular steroidogenic activity has been studied by testing the capacity of conditioned medium (CM) by both unstimulated (control) Sertoli cells (C-CM) and FSH stimulated Sertoli cells (FSH-CM) to influence porcine cultured Leydig cell activity. Leydig cells cultured in FSH-CM for 48 hrs, as compared to C-CM, show a significant (P less than 0.05) increase in [125I]-hCG binding (150% +/- 4) and hCG-stimulated testosterone (T) secretion (266% +/- 42). In addition, the stimulating effect of FSH-CM on Leydig cell function as compared to C-CM, is trypsin sensitive, non dialyzable, heat stable, acid resistant and is chromatographed following gel filtration (Sephadex G 100) into two different peaks of activity. These data suggest that FSH regulates Leydig cell function via (at least two types of) Sertoli cell secreted proteins.

Animals↗
PubMed1983

Role of FSH and oestradiol-17 beta in the development of meiotic competence in rat oocytes.

The ability of rat oocytes to resume meiotic maturation upon isolation ("meiotic competence") was shown to be abolished by hypophysectomy on day 15 post partum (p.p.). FSH (NIAMD-rat FSH-B-1; 10-20 micrograms/day), but not LH (NIAMD-oLH-21; 2-20 micrograms/day) was able to induce meiotic competence in rats hypophysectomixed on day 15 pp. Implantation of a capsule of oestradiol-17 beta, but not of progesterone or androstenedione, partially restored meiotic competence in hypophysectomized rats within 24 h of treatment. When inhibitors of steroidogenesis (aminoglutethimide, 17 beta-formamidoandrost-4-en-3-one, 1,4,6-androstatriene-3,17-dione or 4-hydroxy-4-androstene-3,17 dione) were coadministered with FSH they inhibited its effect on the development of meiotic competence. Furthermore, when oestradiol-17 beta was administered together with these inhibitors of steroidogenesis, the effect of FSH on the development of meiotic competence was not disturbed. These results strongly suggest that FSH, but not LH, is involved in the development of meiotic competence. Further, this action of FSH appears to be mediated, at least partially, by follicular oestrogen production.

Animals↗
PubMed1990

Similarities and differences in progesterone and androgens in modulation of LH, FSH and PRL release: unexpected properties of flutamide.

The purpose of this study was to determine if the similarity of effect of progesterone and androgens on antagonism of estrogen-induced prolactin release also applied to the regulation of LH and FSH release. An additional objective was to examine the effect of the antiandrogen, flutamide, upon the ability of progesterone to induce gonadotropin secretion. Using the ovariectomized estrogen-primed immature rat, testosterone propionate suppressed LH and FSH secretion, whereas dihydrotestosterone only suppressed serum LH levels. In contrast, progesterone significantly elevated both serum LH and FSH levels. Thus, with respect to regulation of gonadotropin secretion, the effects of androgens and progesterone were dissimilar. In the estrogen-primed ovariectomized immature rat, flutamide was found to suppress LH, FSH and PRL secretion. Progesterone (0.8 mg/kg body wt) was incapable of overcoming this suppressive effect of flutamide. The effect of flutamide on gonadotropin secretion required estrogen priming. The effect of flutamide in suppressing LH, FSH and PRL release was not through suppression of an adrenal steroid as shown by adrenalectomy or the use of RU486. In the PMSG primed immature rat, flutamide had no effect on basal gonadotropin levels or ovulation. However, flutamide antagonized progesterone and triamcinolone acetonide-induced gonadotropin surges and blocked their ability to facilitate ovulation. These studies demonstrate that in the ovariectomized estrogen-primed immature rat flutamide has potent neuroendocrine regulatory ability leading to suppression of LH, FSH and PRL release. Flutamide also blocked progesterone and triamcinolone acetonide induced gonadotropin surges and ovulation in PMSG-primed immature female rats.

Adrenalectomy↗
PubMed1989

Inhibition of FSH-stimulated cAMP accumulation by mono(2-ethylhexyl) phthalate in primary rat Sertoli cell cultures.

High doses of phthalate esters in vivo cause testicular lesions. One initial target for these effects is the sustentacular Sertoli cell. Sertoli cells are unique in that they have surface membrane receptors for follicle-stimulating hormone (FSH), which couple to adenylate cyclase. As a means of investigating why phthalates appear specific for Sertoli cells, we evaluated possible effects of an active monoester [mono(2-ethylhexyl) phthalate, MEHP] on the ability of FSH to elevate intracellular levels of cAMP. MEHP reduced FSH-induced elevation of cAMP levels by approximately 40%. This inhibition by MEHP required a lag period of 6 hr and did not affect the dose of FSH which gave half-maximal stimulation, suggesting that MEHP does not compete with FSH for binding to its receptor. The MEHP inhibition was not affected by incubation in the presence of methylisobutylxanthine, a phosphodiesterase inhibitor, suggesting that MEHP does not stimulate the breakdown of cAMP. The MEHP-induced inhibition is specific for FSH; it does not affect the ability of forskolin, cholera toxin, isoproterenol, or prostaglandin E1 to stimulate Sertoli cell cAMP. Furthermore, inhibition occurs in the presence of pertussis toxin suggesting that MEHP action is independent of the inhibitory adenylate cyclase pathway. Further experiments will be necessary to define the specific mechanism of action of phthalates on Sertoli cells; however, these experiments do describe a specific site of action of MEHP in vitro which may be related to the in vivo testicular toxicity of phthalate esters.

Animals↗
PubMed1985

LH and FSH profiles at superovulation and embryo production in the cow.

The variability of the superovulation response in cattle is an important problem to the commercial embryo transfer industry. Plasma LH and FSH concentrations around the time of estrus and ovulation were studied in relation to embryo production, to try and elucidate this problem. Sixteen cows were superovulated with 38 mg FSH-P and estrus synchronized with prostaglandin F(2) alpha. On the third and fourth day of superovulation increases in plasma LH but not FSH were detected. The LH and FSH profiles appeared to be normal in the size of the surge but in many cases they were were abnormal in timing. Transferable embryo production appeared to be lower in cows in which the LH and FSH surges were not coincident, and in cows where the surges were early or late with reference to estrus. FSH appeared to be primarily responsible for the number of embryos produced and LH for their quality, i.e. the number transferable.

Journal Article↗
PubMed1992

Control of FSH, follicular development and estrus synchronization in the mare with steroid-free follicular fluid.

Twenty-two pony mares were used in a project designed to determine the effectiveness of different treatments in controlling FSH, follicular development and synchronization of estrus and ovulation. Mares in Group 1 (n=8) received daily oral altrenogest (0.044 mg/kg); those in Group 2 (n=7) received daily altrenogest (0.044 g/kg) and, during the last 4 days of treatment they received steroid-free follicular fluid, (15 cc) intravenously (I.V.) two times a day; Mares in Group 3 (n=7) received daily intramuscular (I.M.) injections of progesterone (80 mg) and estradiol valerate (7 mg). All treatments lasted for 10 days, at the end of which prostaglandin (PgF(2)alpha, 10 mg) was administered. Sexual behavior, follicular development and FSH concentrations were monitor daily. Concentrations of FSH in Group 2 mares, were not significantly different (P>0.05) from those of Group 1 until the mares in Group 2 were treated with follicular fluid (P<0.05). Concentrations of FSH in Group 3 mares, were significantly lower than those of Groups 1 and 2 (P<0.05) until the mares in Group 2 were treated with steroid-free follicular fluid. At this point there was no significant difference between groups 2 and 3 (P>0.05). Steroid-free follicular fluid appears to induce atresia in larger follicles (>11 mm), and the initiation of new follicular wave. The combination of progesterone and estradiol valerate appears to delay follicular growth and not to induce atresia, since larger follicles (>11 mm) continued to grow after treatment. Both treatments (groups 2 and 3) resulted in ovulations within 5 days period. The treatment in Group 1 did not have any effect on FSH or follicular development and ovulations were dispersed through a 9-day period. We concluded that steroid-free follicular fluid offers a new possibility to synchronize ovulation in the mare by controlling FSH and follicular development.

Journal Article↗
PubMed1993

Simultaneous injection of follicle stimulating hormone (FSH) and the prostaglandin F2alpha analog cloprostenol (PGF) disrupts follicular activity in diestrous dairy cows.

Simultaneous injections of PGF and FSH or saline were given to 32 Holstein cows to test their combined ability to improve estrous and ovulation synchrony beyond that of PGF alone. All the cows were randomly assigned to receive PGF on either Day 8 or Day 10 of the estrous cycle (estrus = Day 0), and all the cows in each group were further assigned to simultaneous injection of either FSH or saline. Regression of the corpus luteum (CL), return to estrus and follicular activity were monitored by plasma progesterone assay, twice-daily estrous detection and ultrasonographic examination, respectively. Plasma progesterone concentrations declined to <1.0 ng/ml at 24 hours after PGF treatment in all the cows and FSH did not affect this decline. Return to estrus was not affected by FSH treatment in cows treated on Day 8 or Day 10; however, FSH disrupted normal follicular activity and either delayed normal ovulation following estrus or induced premature ovulation or cyst formation in 4 of 8 PGF/FSH (Day 8) cows and 5 of 8 PGF/FSH (Day 10) cows. These data indicate that exogenous FSH administered simultaneously with a luteolytic does of PGF does not maintain viability of large, dominant follicles and, therefore, is not an effective method for the synchronization of estrus and ovulation.

Journal Article↗
PubMed1993

Relationships between FSH surges and follicular waves during the estrous cycle in mares.

Individual follicles >/=15 mm were monitored daily by ultrasonography in 12 mares during the estrous cycle. Follicular waves were designated as major waves (primary and secondary) and minor waves based on maximum diameter of the largest follicle of a wave (major waves, 34 to 47 mm; minor waves, 18 to 25 mm). Dominance of the largest follicle of major waves was indicated by a wide difference (mean, 18 mm) in maximum diameter relative to the second largest follicle. Dominant follicles of primary waves (n=12) emerged (attained 15 mm) at a mean of Day 12 and resulted in the ovulations associated with estrus (ovulation=Day 0). The dominant follicle of a secondary wave (n=1) emerged on Day 2 and subsequently ovulated in synchrony with the dominant follicle of the primary wave, which emerged on Day 9. The largest follicles of minor waves (n=4) emerged at a mean of Day 5, reached a mean maximum diameter 3 days later, and subsequently regressed. There was a significant increase in mean daily FSH concentrations either 6 days (primary wave) or 4 days (minor waves) before the emergence of a wave. Mean concentrations of FSH decreased significantly 2 days after emergence of the primary wave. Divergence between diameter of the dominant and largest subordinate follicle of the primary wave was indicated by a significantly greater mean diameter of the dominant follicle than of the largest subordinate follicle 3 days after wave emergence and by the cessation of growth of the largest subordinate follicle beginning 4 days after the emergence of a wave. Surges of FSH were identified in individual mares by a cycle-detection program; surges occurred every 3 to 7 days. Elevated mean FSH concentrations over the 6 days prior to emergence of the primary wave was attributable to a significantly greater frequency of individual FSH surges before wave emergence than after emergence and to an increase in magnitude of peak concentrations of FSH associated with individual surges.

Journal Article↗
PubMed1995

Pulsatile release of FSH for superovulation in cattle.

The studies reported here were directed towards the development of an implantable microcapsule which "pulses" release of follicle stimulating hormone, FSH, for application to superovulating cows. Final dose forms were administered using membrane-coated cylinders. The "pulse" of the FSH is achieved by membrane encapsulation of an effervescent/swelling core containing citric acid, sodium bicarbonate, glucose and FSH. Entry of water results in sufficient pressure increase (by gas generation) to rupture ("burst") the membrane. Time to rupture is dependent upon several factors, such as membrane permeability and thickness, and core composition and loading. The final dose forms were implanted by means of a trochar. This system was tested in sheep to substantiate in vivo "burst" times and then tested in cows to determine efficacy. In vivo burst times in sheep varied from 8 to 96 hr, based upon maximal FSH values in blood serum, and generally paralled the planned times resulting from in vitro tests. Multiple capsules designed to release FSH as a pulse or steady state were tested on a limited number of cows plus a control (n = 10). Four of the combinations resulted in 11, 11, 14 and 16 ovulations, indicating that further development has promise of providing a one-injection system using FSH for superovulating cattle.

Journal Article↗
PubMed1995

Associations between emergence of follicular waves and fluctuations in FSH concentrations during the estrous cycle in ewes.

Folliculogenesis was studied daily in 16 interovulatory intervals in 5 Polypay ewes from mid February through April using transrectal ultrasonic imaging. The 3-mm follicles attaining > or = 5 mm on Days--1 (ovulation=Day 0) to 11 showed significant peak numbers on Days 0, 5 and 10. The number of 3- and 4-mm follicles that did not reach > 4 mm was not significant, indicating that these follicles did not manifest a wave pattern. A follicular wave was defined as one or more follicles growing to > or = 5 mm; the day the follicles were 3 mm was the day of wave emergence, and the first wave after ovulation was Wave 1. Waves 1, 2 and 3 emerged on Days -1 to 2,4 to 7 and 8 to 10, respectively. Four interovulatory intervals in April were short (9 to 14 d), indicating the end of the ovulatory season. In the remaining 12 intervals, the ovulatory wave was Wave 3 in one interval, Wave 4 in 8 intervals, and Wave 5 or 6 in 3 intervals. The ovulatory wave followed the rhythmic pattern of Waves 1 to 3 by emerging on Days 11 to 14 in 50% of the intervals. In the remaining intervals, either the ovulatory wave was Wave 4 but did not emerge until Day 16 or other waves intervened between Wave 3 and the ovulatory wave. The longest intervals (22, 24 and 24 d) had >4 waves. Based on a cycle-detection program, peak values of FSH fluctuations were temporally associated with the emergence of waves as indicated by the following: 1) tendency (P < 0.08) for an increase in FSH concentrations between 3 and 2 days before emergence of a wave; 2) close agreement between mean number of waves per interval (mean +/- SEM, 4.1 +/- 0.3) and mean number of identified FSH fluctuations (4.5 +/- 0.3); 3) close agreement in length of interwave intervals (4.0 +/- 0.3) and interpeak (FSH) intervals (3.6 +/- 0.2); 4) positive correlation (r(2)=0.8) for number of the 2 events (follicular waves and FSH fluctuations) within intervals; and 5) a closer (P < 0.01) temporal relationship between the 2 events than would have been expected if the events were independent. The results support a relationship between transient increases in FSH concentrations and emergence of follicular waves throughout the interovulatory interval in Polypay ewes, with the 2 events occurring approximately every 4 d.

Journal Article↗
PubMedDate not supplied

Effects of the gonadotropin-releasing hormone associated peptides (GAP) on the release of luteinizing hormone (LH), follicle stimulating hormone (FSH) and prolactin (PRL) in vivo.

Six peptide sequences residing between basic amino acid residues in GAP were tested for effects on the release of FSH, LH and PRL in vivo in ovariectomized, estrogen-progesterone-primed (OEP) rats. Synthetic GAP peptides (1-13, 1-23, 15-23, 25-36, 38-53 and 41-53) were injected intravenously (IV) into conscious OEP rats and plasma levels of FSH, LH and PRL were measured by RIA. The activity of GAP peptides in the control of PRL was further examined in ether-stressed male rats which were injected IV with GAP peptides just prior to a 1-min etherization. GAP(1-13) significantly stimulated FSH release at doses of 1, 10 and 100 micrograms, whereas it stimulated LH release only at the highest dose of 100 micrograms. GAP(1-23) elevated plasma levels of FSH and LH only at a dose of 100 micrograms. The other 4 peptides had no effect on the release of gonadotropins. Of these 6 peptides, only GAP(1-13) partially lowered the plasma levels of PRL at the high dose of 100 micrograms in OEP rats, but it had no effect on the ether-induced PRL surge at doses of 10 and 100 micrograms. In conclusion, both GAP(1-13) and GAP(1-23) stimulate FSH and LH release in vivo; these 2 peptides are much less potent in stimulating gonadotropin release than is LHRH. GAP(1-13) exerts a preferential FSH-releasing activity, but its PRL-inhibiting activity is minimal.

Animals↗
PubMedDate not supplied

Similarity of responses of cultured Sertoli cells to cholera toxin and FSH.

The effects of cholera toxin on the responses of cultured Sertoli cells were compared with those elicited by follicle-stimulating hormone (FSH), and N6O2'-dibutyryl-3',5'-cyclic AMP (bu2cAMP). Addition of FSH or cholera toxin increased cAMP levels. Subsequently there was greater rates of conversion of testosterone to 17beta-estradiol, formation of androgen-binding protein (ABP), and incorporation of [3H]thymidine into DNA by Sertoli cells prepared from testes of immature rats and cultured in the presence of either FSH or cholera toxin. Addition of bu2-cAMP also resulted in enhanced rates of formation of ABP, synthesis of 17beta-estradiol and synthesis of DNA. Cholera toxin and bu2-cAMP elicited changes in morphology of cultured Sertoli cells indistinguishable from those following FSH addition. It is concluded that elevated intracellular cAMP levels can duplicate known actions of FSH on cultured Sertoli cells, but the possible obligatory role of cAMP in mediating FSH actions remains to be evaluated.

Animals↗
PubMedDate not supplied

A synergistic effect of androgen on the stimulation of progesterone secretion by FSH in cultured rat granulosa cells.

Granulosa cells from preovulatory follicles (PO) or from the enlarged preantral follicles of hypophysectomized immature diethylstilbestrol-treated (Hx-DES) rats were cultured with various combinations of FSH, androst-4-ene-3,17-dione (Ad), estradiol-17beta and dibutyryl cyclic AMP (dbcAMP). Progestin levels (progesterone and 20alpha-dihydroprogesterone) in the medium after 2 days of culture were assayed by radioimmunoassay. The control levels of the two progestins were lower for Hx-DES than for PO cells. Rat FSH (NIAMD-1-3;0.1 mug/ml) caused a 2-fold rise in progestin accumulation in both PO and Hx-DES cultures, dbcAMP (1 mM) increased progestin accumulation in PO cultures 4-5-fold, and to an even greater extent (10-20 fold) in Hx-DES cultures. Androstenedione (1.0 mug/ml) augmented progestin accumulation (1.5-3-fold), and synergized the steroidogenic action of FSH: in cells from Hx-DES rats, combined treatment with FSH and Ad caused a 5-10-fold increase over the values obtained with FSH alone. Testosterone and 5alpha-dihydrotestosterone, but not estradiol-17beta or estrone, mimicked these effects of Ad, Ad did not synergize the action of dbcAMP on progestin levels in Hx-DES cultures. It is proposed that androgen may play a role in the development of the FSH-responsive mechanism in preantral granulosa cells.

Androgens↗
PubMed1977

Studies on the synergistic effect of androgen on the stimulation of progestin secretion by FSH in cultured rat granulosa cells: a search for the mechanism of action.

Cultures of granulosa cells from immature hypophysectomized DES-treated rats were unable to maintain progestin production of more than 48 h in medium without hormone supplementation or in the presence of FSH only. Production of progestin (20alpha-dihydroprogesterone, as measured by radioimmunoassay) remained unimpaired in the presence of androstenedione (Ad) and was markedly increased in the presence of both Ad and FSH. The combined treatment with FSH and Ad during the first 48 h of culture brought about persistent changes in the cultured cells, since progestin accumulation did not decline upon subsequent removal of these hormones during days 3 and 4 of culture. Dibutyryl cyclic AMP (DBC) was able to mimic the changes in steroidogenic capability induced by the combined action of FSH and Ad. The extent of [125I]-FSH binding, FSH-stimulable cAMP accumulation and cyclic 3',5'-nucleotide phosphodiesterase activity were not affected by addition of Ad to the culture medium. Ad synergized with DBC in the stimulation of progestin accumulation in granulosa cell cultures. It is suggested that androgen acts at a step in the regulation of progestin biosynthesis distal to cAMP production.

20-alpha-Dihydroprogesterone↗
PubMed1981

FSH induction of aromatase in cultured rat granulosa cells measured by a radiometric assay.

The effects of FSH on the aromatase activity of rat granulosa cells in culture were studied by measuring the stereospecific transfer of 3H from [1,2,6,7-3H]testosterone or [1 beta-3H]testosterone into 3H2O. The use of 3H2O release as a specific assay for aromatization in granulosa cells was validated by various means. 2 days after plating, cultures of granulosa cells released only minimal amounts of 3H2O from [1 beta-3H]testosterone during a 3-h incubation, whereas cells which had been treated with FSH, or with (Bu)2cAMP plus 3-isobutyl-1-methylxanthine (MIX), from the time of plating released considerable amounts of 3H2O into the culture medium. The release of 3H2O from [1 beta-3H]testosterone by cultured cells was inhibited by the aromatizable androgens, 19-hydroxytestosterone and 19-hydroxyandrostenedione, indicating the specificity of the method for aromatization. In order to study the mechanism by which FSH enhanced the release of 3H2O, optimal conditions for aromatization by cell-free sonicates were determined. Optimal aromatase activity was achieved by incubating cell-free sonicates at 37 degrees C in the presence of O2 in 20 mM phosphate buffer (pH 7.4) containing 5 mM dithiothreitol, 20 mM MgCl2, 0.5 mM NADP+, 20 mM glucose 6-phosphate and 2 U/ml glucose-6-phosphate dehydrogenase. A concentration of 0.25 microM testosterone and 0.1 microCi tritium was used in the standard assay. Under these conditions the assay was linear for 1 h with up to 150 microgram protein from granulosa cells having maximal aromatase activity. When cells in culture were stimulated with purified FSH for 48 h from the time of plating, the aromatase activity in cell-free sonicates increased in a dose-dependent fashion. The ED50 for Sairam's FSH S-1528 C2 was 12 ng/ml. It was concluded from these studies that FSH increases estrogen levels primarily by inducing an active aromatase rather than by influencing secretion or availability of substrate or cofactor for the aromatization reaction.

1-Methyl-3-isobutylxanthine↗
PubMed1982

Inhibition of FSH action on granulosa cells by low molecular weight components of follicular fluid.

Immature female rats were injected with a single dose (10 IU) of pregnant mare serum gonadotropin to induce growth and maturation of ovarian follicles. Using such ovaries as a model, we tested the effects of low molecular weight subfractions of charcoal-absorbed bovine follicular fluid (FF-c) on (a) radioiodinated human FSH (125I-hFSH) binding to ovarian homogenates, (b) ovine FSH-stimulated adenylate cyclase activity in granulosa cell homogenates and (c) cAMP production by intact granulosa cells. The follicular fluid was fractionated by ultrafiltration through membranes of differing pore-sized into molecular weight components of 1000-5000 (passing Amicon H1P-5 hollow fibers but retained by Amicon UM-2 membrane) and 500-1000 (passing Amicon UM-2 membrane but retained by Amicon Um-05 membrane). These low molecular weight fractions inhibited 125I-hFSH binding to ovarian receptors, FSH-stimulated cAMP production by rat granulosa cells and FSH-stimulated, as well as fluoride-ion-stimulated adenylate cyclase activity in granulosa cell homogenates. Inhibition of FSH-stimulated adenylate cyclase activity by the FF subfractions was non-competitive as determined by double reciprocal plot analysis. Our results suggest that modulation of FSH effects on granulosa cells may be mediated by low molecular weight constituents of follicular fluid.

Adenylyl Cyclase Inhibitors↗
PubMed1983

Proteoglycan production by bovine granulosa cells in vitro occurs in response to fsh.

Bovine granulosa cells from small (1-9 mm) or large (10-20 mm) follicles were incubated in a chemically defined medium containing 5 muCi/ml [3H]glucosamine, gonadotropins or polypeptide hormones, 8-Br-cAMP, theophylline or trifluoperazine (TFP). Radiolabeled proteoglycans were precipitated with 10% phosphotungstic acid. Maximum incorporation of isotope occurred in 45-60 min. Radiolabeled products were completely hydrolyzed with chondroitinase ABC. FSH, but not LH or hCG, yielded a significant log-dose response. High doses of hCG inhibited the ability of granulosa to respond to FSH. No other hormone altered the FSH dose-response curve. Addition of 8-Br-cAMP or theophylline mimicked the FSH response. The FSH effect was blocked by TFP, an inhibitor of calmodulin, but cAMP or theophylline overcame the effect of TEP. No distinct difference in response to these various compounds was noted between granulosa from small or large follicles. This system provides a biochemical marker for evaluating a mechanism of action for FSH.

8-Bromo Cyclic Adenosine Monophosphate↗