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PubMed1990

Mouse oocytes regulate hyaluronic acid synthesis and mucification by FSH-stimulated cumulus cells.

Mucification (or expansion) of the cumulus cells surrounding the oocyte is thought to depend on the direct action of gonadotropins in stimulating production and deposition of hyaluronic acid (HA) in the extracellular matrix. We now report that the oocyte is essential for this process. Either follicle-stimulating hormone (FSH) at 1 micrograms/ml or dibutyryl cAMP at 2 mM induces mucification of intact cumulus cell-oocyte complexes (COCs) in vitro, but fails to stimulate mucification of isolated cumulus cells. HA synthesis by FSH-stimulated cumulus cells is only approximately 3.5% of the value achieved by FSH-stimulated COCs. Isolated oocytes cultured with or without FSH do not synthesize detectable amounts of HA but induce isolated cumulus cells to increase HA synthesis approximately 13-fold in cocultures with FSH. Medium conditioned by isolated oocytes for 5 hr induces nearly the same level of HA synthesis by cumulus cells under the same culture conditions. FSH also stimulates cumulus cells to increase synthesis of dermatan sulfate proteoglycans (DS-PGs) approximately 3-fold, but this stimulation does not depend upon the presence of oocytes. The results indicate that oocytes produce a soluble factor(s) essential in combination with FSH to stimulate HA, but not DS-PG, synthesis by cumulus cells in vitro and that this factor(s) acts independently or downstream from the FSH-induced formation of cAMP.

Animals↗
PubMed1976

LH and FSH responses to luteinizing-releasing hormone in normal, adult, human males.

Time-response and dose-response relationships were established for the LH and FSH response to single intravenous bolus injections of synthetic LRH. Sixteen normal adult human males, ages 19-45 were studied, and 80 individual tests were performed using a broad range of LRH doses from 0-3000 mug. Serum gonadotropins were measured at frequent intervals ranging from -30 to 180 min after LRH injection. The curves describing changes in blood LH and FSH with time were not superimposable at any dose level. The 50% decay time for the LH response showed a significant linear log-dose relationship to LRH. For LH, dose-response relationships existed for both, the peak LH release, and the total LH secretion (area under the time-response curve). No minimal or maximal effective doses were reached for LH within the dose range from 1 to 3000 mug LRH. The smallest dose (measured as peak LH concentration), that produced a response significantly different from saline injections, was 1.58 mug/subject; judged by total LH secretion (area under the time-response curve) the smallest dose producing a significant response was 2.39 mug/subject. No dose-response relationship existed for the peak FSH release. Judged by total FSH secretion (area under the time-response curve), the effects of LRH were dose related; the smallest effective dose was 20 mug LRH. As for LH, no maximal effective dose was reached within the dose range studied. The 95% confidence intervals for the peak responses to an intravenous bolus injection of 100 mug synthetic LRH were 400%-800% of the individual mean base line LH concentration, and 100%-200% of the individual mean base line FSH concentration. Serum testosterone did not change significantly in response to single bolus injections of LRH at any of the dose levels studied. The peak LH responses to any dose of LRH were positively correlated to the individual mean base line LH concentrations. No correlations were observed between the peak LH or FSH responses and age, race, marital status, body weight, or body surface area of the subjects. In a second series of studies, a 2-hr, constant infusion of synthetic LRH was administered at five different infusion rates (doses) to four normal adult human males for a total of 20 infusions. Serum LH and FSH responses were sustained at dose related levels characteristic of each individual during the entire LRH infusion period. In contrast to the lack of testosterone responses to bolus injections of LRH, serum testosterone rose significantly in response to all dose levels of LRH infusion. These are the most extensive pharmacologic studies of LRH-LH and LRH-FSH relations in man yet reported.

Adult↗
PubMed1988

Predictive value of the FSH:LH ratio on follicular and luteal phase characteristics of the human menstrual cycle.

A prospective study was designed to assess the predictive value of gonadotropin measurements obtained during the early follicular phase upon the hormonal characteristics of the subsequent cycle. The data obtained in 12 normal cycles were used to compute the mean and confidence interval (mean +/- 2 SEM) of the FSH:LH ratio, FSH and LH plasma levels. The limits of the confidence intervals for these different parameters were used to classify the patients. Data of 204 patients were analysed. Low FSH:LH ratios (less than 1.34) are associated with an increase in follicular phase length (+2.4 days), a lower ovulatory rate, but neither luteal phase length nor progesterone levels differ between these two groups. When patients are classified according to FSH levels, our results show that low FSH levels (less than 2.94 mIU/ml) are associated with longer follicular (+2.6 days) and shorter (-1.1 days) luteal phase lengths, but ovulatory rate and progesterone levels in the luteal phase of the ovulatory cycles are similar to those obtained in patients of the normal or high FSH group. High LH levels (greater than 3.15 mIU/ml) are associated with a decreased ovulation rate but follicular and luteal phase characteristics are similar to those obtained in patients in the normal or low LH group. In conclusion, low FSH: LH ratios and low FSH plasma levels measured in the early follicular phase of the cycle are associated with longer follicular phase lengths; but basal gonadotropin measurements have limited predictive value on luteal phase characteristics.

Female↗
PubMed1989

Ultrasonographic determination of ovarian follicular. Development in superovulated heifers pretreated with FSH-P at the beginning of the estrous cycle.

On Day 3 of the estrous cycle (estrus = Day 0), dairy heifers were given either 10 mg i.m. FSH-P (FSH-P primed; n = 9) or a saline vehicle (saline primed; n = 9). On Day 10, all heifers were superovulated with FSH-P (total = 27.7 mg i.m.) in declining doses over 5 d. Heifers were inseminated artificially at estrus. From Day 2 until estrus, the number and size of follicles >2 mm were monitored daily by ultrasonography. The mean (+/- SEM) number of corpora lutea (CL) (6.2 +/- 1.5 vs 10.7 +/- 0.9; P<0.05) and the mean number of recovered embryos and unfertilized ova (3.6 +/- 1.7 vs 8.4 +/- 2.2; P<0.05) were lower in FSH-P-primed than in saline-primed heifers. Prior to initiation of superovulation, follicles >10 mm appeared on Days 6 to 7 in saline-primed heifers but only on Days 8 to 10 in FSH-P-primed heifers (P<0.05). Also, until Day 10, the mean number of follicles 4 to 6 mm and 7 to 10 mm was higher (P<0.05) in FSH-P-primed than in saline-primed heifers. After initiation of the superovulatory treatment (Day 10 to estrus), saline-primed heifers had a greater and faster increase in the mean number of follicles >10 mm (P<0.02) than FSH-P-primed heifers did. Depletion in the number of follicles 2 to 3 mm (P<0.001) between Day 10 and estrus and in the number of follicles 4 to 6 mm (P<0.05) between Day 12 and estrus occurred in both groups of heifers. Decreased superovulatory response and embryo recovery in FSH-P-primed heifers may have been due to the presence of large follicles (>10 mm) prior to the initiation of the superovulatory treatment which reduced the ability of small follicles to grow into larger size classes during superovulatory treatment.

Journal Article↗
PubMed1991

Superovulation of dairy cows with purified FSH supplemented with defined amounts of LH.

This study investigated the effects of a purified follicle stimulating hormone (FSH) preparation supplemented with three different amounts of bovine luteinizing hormone (bLH) and a commercially available FSH with a high LH contamination on superovulatory response, plasma LH and milk progesterone levels in dairy cows. A total of 112 lactating Holstein-Friesian crossbred dairy cows were used for these experiments; the cows were randomly assigned to treatment groups consisting of purified porcine FSH (pFSH) supplemented with bLH. Group 1 was given 0.052 IU LH/40 mg armour units (AU) FSH (n = 6); Group 2 was given 0.069 IU LH (n = 32); Group 3 received 0.423 IU LH (n = 34); while Group 4 cows (n = 36) were superovulated with a commercially available FSH-P. This compound appeared to contain 8.5 IU LH/40 mg AU FSH according to bioassay measurement. All animals received a total of 40 mg AU FSH at a constant dose twice daily over a 4-d period. Levels of milk progesterone and plasma LH were determined during the course of superovulatory treatment. The Group 1 treatment did not reveal multiple follicular growth, and no embryos were obtained. Superovulation of Group 3 cows resulted in significantly (P<0.05) more corpora lutea (CL; 12.6+/-1.1) and fertilized ova (5.1+/-1.3) compared with Groups 2 and 4 (10.1+/-0.9 and 2.6+/-0.6, 9.0+/-0.9 and 2.7+/-0.5, respectively). Due to a high percentage of degenerated embryos (33%) Group 3 yielded only one more transferable embryo than Groups 2 and 4. Among groups, LH levels differed in the period prior to induction of luteolysis and were similar thereafter. The progesterone pattern following FSH/LH administration reflected the amount of LH supplementation. Milk progesterone levels on the day prior to embryo collection were correlated to the number of CLs and recovered embryos. It is concluded that under the conditions of our experiment superovulation with 0.423 IU LH/40 mg AU FSH may yield a significantly improved superovulatory response in dairy cows. It is further suggested that LH supplementation exerts its effects mainly on follicular and oocyte maturation during the period prior to luteolysis.

Journal Article↗
PubMed1994

FSH-stimulated follicular secretions enhance oocyte maturation in pigs.

Follicular secretions can support cytoplasmic maturation in vitro in the pig. The effects of follicular secretions stimulated in vitro by different combinations of gonadotropins and over different culture periods on cytoplasmic maturation of the pig oocyte were studied. In Experiment 1, follicular shells (including theca and mural granulosa cells) from 5 to 7-mm follicles were cultured in vitro under the stimulation of different combinations of gonadotropins for 48 h, and then the obtained conditioned media were used for oocyte maturation. Oocytes cultured in conditioned medium harvested after treatment of follicular shells with 2.5 mug/ml FSH (FSH-stimulated conditioned medium) yielded a higher percentage of male pronuclear formation than those matured in conditioned medium harvested after culture of follicular shells with a combination of hormones (2.5mug/ml FSH, 2.5 mug/ml LH and 20 ng/ml PRL, FSH-LH-PRL-stimulated conditioned medium; 54.1 vs 28.5%; P=0.001). Addition of the combination of FSH, LH and PRL during the period of oocyte maturation marginally improved male pronuclear formation rates (41.3 vs 55.6%; P=0.06). In Experment 2, follicular shells were cultured under the stimulation of FSH only. Conditioned media were harvested after the first 24 h and the second 24 h of culture. The rates of male pronuclear formation in oocytes matured in these 2 conditioned media did not differ (P=0.65), but were higher than those of oocytes matured in fresh control medium (P<0.03). It is concluded that factors secreted by follicular cells stimulated by FSH alone provide better support for full oocyte maturation in the pig than by combined FSH, LH and PRL treatment.

Journal Article↗
PubMed1989

Developmental changes in FSH secretion induced by 5-hydroxytryptophan, naloxone and haloperidol in male and female rats.

Follicle-stimulating hormone (FSH) secretion is increased in the immature female rat from day 5 to days 17-18 of life, and decreases steadily thereafter until puberty. It has been reported that estradiol negative feedback and inhibin-like peptides are low during this period, while luteinizing hormone (LH) and FSH sensitivity to LH-releasing hormone (LHRH) are maximal. It was therefore of interest to study the effects of some neurotropic drugs on FSH release at 12 days of age, and to compare their effects at 1 and 20 days. Besides, as developmental patterns and regulation of FSH are different in male and female rats, the experiments were carried out using male and female littermates. The drugs chosen were haloperidol, 5-hydroxytryptophan and naloxone. These drugs release LH in the infantile female rat, the effect decreasing or disappearing as the animal matures; no effects of these drugs have been reported on FSH release in infantile rats to the present time. It was found that haloperidol (0.25 mg/kg), naloxone (2 mg/kg) and 5-hydroxytryptophan (50 mg/kg) markedly increased the already high titers of FSH in the 12-day-old female rat. This effect could not be discerned in newborn rats, and had disappeared at 20 days of age. Male littermates failed to respond at any age. When adult male and female rats in diestrus were tested, all drugs at the chosen doses were ineffective in altering FSH release. These data suggest that the infantile female rat represents an interesting physiological model to evaluate the neural regulation of FSH in a situation in which inhibitory signals provided by inhibin and estrogen in later life are diminished.

5-Hydroxytryptophan↗
PubMed1981

Modulation of FSH-controlled steroidogenesis in rat granulosa cells: direct in-vitro effects of LHRH and ICI-118630.

Direct inhibitory effects of LHRH and an LHRH agonist (ICI-118630) on FSH-controlled steroidogenic processes in ovarian granulosa cells were characterized in vitro. Over a 2-day culture period in the presence of testosterone (10(-7) M), FSH (3-3 000 ng/ml) caused dose-dependent increases in the aromatase activity of granulosa cells isolated from oestrogen-pretreated immature rats. Progestogen biosynthesis was stimulated in a similar manner. The presence of LHRH (10(-9) - 10(-7) M) in the culture medium inhibited these responses by right-shifting the dose-response curves. Thus the net effect was one of reduced sensitivity to FSH. ICI-118630 was approximately 10 times more effective than LHRH as an inhibitor of aromatase induction and progestogen biosynthesis in response to FSH. Over a 1-h incubation at concentrations up to 10(-7) M, neither decapeptide had a consistent inhibitory effect on FSH-stimulated granulosa cell cAMP formation either in the presence or absence of 1-methyl-3-isobutyl-xanthine (MIX); but during the 2-day culture, ICI-118630 and occasionally LHRH significantly inhibited aromatase induction by cholera toxin and 2 different cAMP analogues. Over the same range of concentrations, each peptide progressively inhibited the stimulatory effect of MIX on FSH-induced aromatase activity and progestogen biosynthesis. Thus LHRH/ICI-118630 can directly modulate FSH-controlled granulosa cell steroidogenesis in vitro via effects on one or more biochemical loci distal to the FSH-receptor coupled adenylate cyclase system. These experiments have implications for the role of a putative LHRH-like ovarian substance(s) in the local co-ordination of follicular development and function.

Animals↗
PubMed1982

Progestins inhibit FSH-induced functional LH receptors in cultured rat granulosa cells.

The role of intraovarian progesterone in the control of follicular growth and development remains unclear. The presence of a rat ovary granulosa cell progesterone receptor suggests that progesterone has a direct effect on the follicles. We have previously reported that progestins inhibit FSH-stimulated estrogen production by cultured granulosa cells by inhibiting the FSH induction of the aromatase enzyme. We now report that progestins can inhibit another FSH action on rat granulosa cells; the induction of LH/hCG receptors. The concomitant administration of 10(-5) M R5020, a potent synthetic progestin, with 10 ng/ml FSH during a 2-day culture period inhibits the FSH induction of LH/hCG receptors by 75 +/- 6% (mean +/- S.E.) The progestin inhibition of the induction of LH/hCG receptors is not mediated by its inhibitory action on the induction of aromatase. Scatchard analysis indicates that progestin decreases the number of LH/hCG receptors per cell but has no effect on receptor affinity. Both R5020 and progesterone have a dose-dependent inhibitory effect on the FSH induction of LH/hCG receptors, causing a 30 and 85% decrease in receptor number at concentrations of 10(-6) and 10(-5) M, respectively. The concomitant administration of R5020 with FSH also leads to a significant decrease in the ability of LH to stimulate cAMP production, indicating that progestin is inhibiting the induction of 'functional' LH/hCG receptors. R5020 (10(-5) M) also inhibits by 90% the induction of LH/hCG receptors by cholera toxin and dibutyryl cAmP, indicating that the progestin effect is at a post-cAMP site. Since the induction of LH/hCG receptors by FSH is a necessary event in follicular maturation, these results offer another mechanism by which progestins, at high concentrations, can inhibit follicular growth and development.

Animals↗
PubMed1984

Insulin enhances FSH-stimulated steroidogenesis by cultured rat granulosa cells.

Experimentally induced diabetes in female rats is associated with decreased ovarian functions. We have investigated the ovarian action of insulin using granulosa cells obtained from immature hypophysectomized, estrogen-treated rats. The cells were cultured for 2 days in a serum-free medium in the presence of follicle-stimulating hormone (FSH), with or without insulin. Medium steroids were determined by specific radioimmunoassay. Treatment with FSH caused a dose-dependent increase in the production of estrogen, progesterone, 20 alpha-hydroxypregn-4-en-3-one (20 alpha-OH-progesterone) and pregnenolone. Concomitant treatment with 100 ng/ml insulin increased the responsiveness of granulosa cells to FSH, decreasing the ED50 values for FSH-stimulated estrogen and progestin production 2-2.75-fold. A lower dose of insulin, 10 ng/ml, also augmented FSH action. In contrast, treatment with insulin alone had no effect on steroid production. The insulin effect on progestin and estrogen biosynthesis was detected by 24 and 44 h after treatment, respectively. Also, the insulin action appeared to be specific since an insulin fragment, desoctapeptide insulin, exhibited no effect. Insulin also increased the FSH-stimulated increase in activity of 3 beta-hydroxysteroid dehydrogenase, the rate-limiting enzyme in the formation of progesterone, but was without effect on the activity of 20 alpha-hydroxysteroid dehydrogenase, which converts progesterone to the inactive 20 alpha-OH-progesterone. The effects of insulin on increasing FSH responsiveness could not be accounted for by changes in cell viability or total cell number. These results indicate that insulin exerts a specific action on granulosa cells to increase the FSH stimulation of estrogen and progestin production.(ABSTRACT TRUNCATED AT 250 WORDS)

20-Hydroxysteroid Dehydrogenases↗
PubMed1985

Minimal quantities of FSH beta subunit are released by rat anterior pituitary cells in primary culture.

FSH beta in the medium and extracts of cultured rat anterior pituitary cells was quantitated with a heterologous radioimmunoassay utilizing anti-rFSH beta and hFSH beta as the standard and tracer. After 4 days in culture, extracts were prepared from washed cells, cells incubated for 6 h or 24 h in fresh medium or cells incubated for 6 h in the presence of 10(-7) M GnRH. FSH beta/rFSH molar ratios were approximately 0.05, 0.04, 0.21 and 0.35, respectively. The elevation in FSH beta/rFSH molar ratios in 24 h basal and GnRH-treated cultures was due in part to an increase in intracellular FSH beta. Both unstimulated and GnRH-treated cultures contained non-detectable quantities of FSH beta in the medium (less than 0.063 ng/100 000 cells; FSH beta/rFSH molar ratio less than 0.024). Thus, it appears that cultured rat anterior pituitary cells contain a small amount of uncombined FSH beta but that minimal quantities are released. Furthermore, GnRH may increase intracellular quantities of FSH beta but does not induce its release.

Animals↗
PubMed1993

Effects of adenosine analog PIA (n-phenylisopropyladenosine) on FSH-stimulated cyclic AMP (cAMP) production in the rat seminiferous epithelium.

In rat seminiferous epithelium, FSH-stimulated cAMP production is cyclically modulated by spermatogenic cells and is highest in stages XIV-V and lowest in stages VII-VIII of the epithelial cycle. Adenosine has been proposed to be an inhibitory paracrine molecule in Sertoli cells. In this paper the effect of adenosine analog n-phenylisopropyladenosine (PIA) on FSH-stimulated cAMP production was studied in staged rat seminiferous tubules. In low responsive stages VII-VIII of the cycle, 100 nM and 10 microM PIA inhibited FSH-stimulated cAMP production by 24% and 28%, respectively. To study whether PIA effect is mediated through Gi-protein, pertussis toxin (PT) pretreatment was used to block the Gi-protein. PT pretreatments of 3 or 18 h caused 42% or 16% elevation in FSH-stimulated cAMP production, respectively. PIA blocked the stimulation caused by PT pretreatment. At 38 days post irradiation, when spermatocytes and round spermatids were decreased in number, in stages VII-VIII of the cycle the inhibitory effect of PIA was abolished. In high responsive stages XIV-V of the cycle, 100 nM PIA stimulated cAMP production by 27%, while 10 microM PIA had no effect. At 38 days post irradiation FSH response was decreased by 19% when compared to non-irradiated level, and PIA stimulated FSH-stimulated cAMP production by 22%. The results suggest that there are stage-specific mechanisms for adenosine-dependent regulation of FSH-stimulated cAMP production in the rat seminiferous epithelium. Advanced spermatogenic cells seem to maintain the mechanisms that include PIA-mediated inhibition of FSH response. Other mechanisms than PT-sensitive Gi-protein seem to be involved in the inhibition.

Animals↗
PubMed1993

Occurrence and de novo biosynthesis of follicle stimulating hormone (FSH) in benign and malignant conditions of human breast.

We report the occurrence as well as biosynthesis of a pituitary hormone, follicle stimulating hormone (FSH) in human breast. Using immunoperoxidase localization technique, both FSH and beta-FSH were localized in cytoplasm of epithelial cells but not in stromal cells. Immunostaining was more intense in benign and malignant specimens as compared to normal. In vitro radiolabelled precursor experiments with breast tissue explants indicate de novo synthesis of FSH. Human milk had higher concentrations of FSH as compared to serum. In gonads, FSH is involved in the cellular growth, differentiation and function. The presence of higher levels of FSH in benign mammary tumors and breast cancer when compared to normal breast supports the suggestion that FSH might have a role in the process of breast malignant transformation.

Breast↗
PubMed1987

Purification of FSH-releasing factor: its dissimilarity from LHRH of mammalian, avian, and piscian origin.

Sheep stalk median eminence fragments were lyophylized, extracted and filtered through a column of Sephadex G-25. The fractions were then assayed for the presence of LHRH by radioimmunoassay (RIA) and bioassayed for FSH and LH-releasing activity following their IV injection into ovariectomized, estrogen progesterone-blocked rats. The radioimmunoassayable LHRH emerged from the column at the same position from which it emerged many years before when LH was measured by bioassay. This same region also contained the LH-releasing activity as measured by bioassay. FSH-releasing activity was present in two tubes just preceding the emergence of the bio- and immunoassayable LHRH. The activity was highly significant and there was no LH-releasing activity in the fractions. They contained much less LHRH as determined by RIA than is sufficient to evoke LH release in this assay. The FSH-releasing activity was recovered in the same fractions in which it was found many years ago with this same assay but with measurement of plasma FSH by bio-rather than immunoassay as employed here. A dose-related release of LH was obtained by injection of LHRH in this assay but there was no significant FSH release even with a dose of 27 ng of LHRH per rat. To determine if one of the LHRHs of lower forms might be FSH-RF, Chicken I and II LHRH and Salmon LHRH were also assayed for FSH- and LH-releasing activity. Each of these peptide possessed LH-releasing activity, albeit much less than that of the mammalian peptide but had no FSH-releasing activity whatsoever.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Effects of cytokines on FSH-induced estradiol production by bovine granulosa cells in vitro: dependence on size of follicle.

The objective of the present studies was to determine the effect of cytokines on FSH-induced estrogen production by granulosa cells from small (1-5 mm) and large (> or = 8 mm) bovine follicles. FSH-induced estradiol production by granulosa cells from large follicles (expressed as pg estradiol/10(5) cells/24 hr) was not affected (P > .05) by 10 or 100 ng/ml of interleukin (IL)-1 beta, 10 or 100 ng/ml of tumor necrosis factor-alpha (TNF alpha) or 100 ng/ml of IL-2. In contrast, 100 ng/ml of IL-1 beta, IL-2 or TNF alpha inhibited (P < .05) FSH-induced estradiol production by 31%, 55% or 72%, respectively in cells from small follicles. Interferon-alpha (IFN alpha; 100 U/ml) inhibited (P < .05) FSH-induced estradiol production by 61% and 20% in cultures of cells from small and large follicles, respectively. Interferon-beta (IFN beta; 100 U/ml), interferon gamma (IFN gamma; 100 U/ml) and bovine trophoblast protein-1 (bTP-1; 100 U/ml) inhibited (P < .05) estradiol production by 47%, 71% and 28%, respectively in cells from small follicles, but had no effect (P > .05) on FSH-induced estradiol production in cells from large follicles. TNF alpha binding protein-I blocked (P < .05) the inhibitory effect of TNF alpha on FSH-induced estradiol production by cells from small follicles. Viability of granulosa cells was not affected (P > .05) by the various cytokines. In summary, cytokines have little or no effect on FSH-induced estradiol production by bovine granulosa cells collected from large follicles, whereas cytokines (bTP-1 < or = IL-1 beta < IL-2 = IFN beta < IFN alpha < TNF alpha) have potent inhibitory effects on FSH-induced estradiol production by granulosa cells collected from small follicles. Thus, it appears that less differentiated granulosa cells (small follicles) are more responsive to cytokines than are highly differentiated granulosa cells (large follicles).

Animals↗
PubMed2005

Cryopreservation of pig granulosa cells: effect of FSH addition to freezing medium.

We cryopreserved swine granulosa cells by a slow cooling rate system; FSH was added to the freezing medium to test its effectiveness in protecting the cells. After thawing, proliferative activity, viability, steroidogenesis and apoptosis were tested; moreover, we determined heat shock protein (HSP70) production, to investigate the recovery from stress and superoxide dismutase (SOD) and catalase activity to evaluate a possible impairment of the antioxidant pathway. E2 production was enhanced by cryopreservation in particular with FSH; on the contrary, P4 production was inhibited by the freezing process in particular without FSH. Only the higher FSH concentration (10 ng/ml) stimulated steroid secretion in freshly collected cells; P4 production by cells cryopreserved in the presence and in absence of FSH was increased by both 5 and 10 ng/ml while the lowest concentration was effective in stimulating E2 production only when FSH was added to freezing medium. Freezing did not modify proliferative activity, while apoptosis was higher in frozen than in fresh cells. HSP70 production was lower in cells cryopreserved in presence of FSH, whose antioxidant metabolism was also conserved: SOD and catalase activities were similar to control. In conclusion, cryopreservation does not seem to markedly affect granulosa cells, in particular if they are frozen in presence of FSH; the gonadotrophin somehow improves their performances after thawing, probably stimulating E2 production and the antioxidant metabolism.

Animals↗
PubMed2006

Evaluation of methodology for administration of porcine FSH for use in estrus induction and for increasing ovulation rate in prepubertal gilts.

Ovulation rate influences production efficiency of oocytes and embryos and depends upon the amount of gonadotropin administered and the ratio of FSH:LH activity. In Experiment 1, gilts (n=135) were assigned to receive 10 or 15 Armour units (AU) of porcine FSH containing 6%, 10%, or 15% LH, whereas controls received PG600. Gilts received 1/6th the FSH dose in six sc administrations at 8-h intervals. There was no treatment effect on incidence of estrus (66%) or cysts (23.9%), or number of corpora lutea (CL, 29.6). However, treatment did affect the percentage of gilts ovulating (P<0.05) with fewer 10 AU FSH with 15% LH-treated gilts ovulating (15%) compared to controls (72%), whereas the other treatments did not differ (range, 44-65%). Experiment 2 tested whether FSH in polyvinlypyrrolidinone (PVP) could induce estrus and ovulation with reduced administration frequency. Gilts (n=105) were assigned to receive 15 AU FSH with 10% LH in one (1P) or two sc administrations (2P) whereas controls received PG600. There was no treatment effect on incidence of estrus (64%) or cysts (22%). However, the percentage of gilts ovulating was lower for 1P (56%), but did not differ (P<0.05) between 2P (83%) and controls (85%). Treatment influenced ovulation rate (P<0.05) with 2P having more CL (24) than controls (12) and 1P (19). Results indicated that 10 and 15 AU FSH induced estrus and ovulation, although high LH content proved detrimental. Further, 15 AU FSH with 10% LH in PVP allowed for reduced administration frequency without compromising ovulation.

Age Factors↗
PubMed2003

FSH and LH-beta subunits in the preoptic nucleus: ontogenic expression in teleost.

In the present study we cloned, sequenced, and confirmed the presence of mRNAs of gonadotropins (FSH-beta, LH-beta subunits) from the brain and pituitary of tilapia, Oreochromis niloticus. Further, we examined the spatio-temporal expression pattern of FSH-beta and LH-beta in the brain and pituitary of two species of teleost (tilapia, O. niloticus; sockeye salmon, Oncorhynchus nerka), using in situ hybridization and immunological methods. The expression of FSH and LH immunoreactivity appeared simultaneously in the brain and pituitary (tilapia, 14 days; sockeye, 51 days after fertilization). In the pituitary, FSH mRNA and peptide expressing cells were distinct from LH expressing cells located in the ventral proximal pars distalis. In the brain, FSH and LH immunoreactivity was co-localized in cells of the preoptic nucleus parvocellularis, magnocellularis, and gigantocellularis. Fibers immunoreactive to FSH and LH antisera were seen along the forebrain-hypothalamus and in the neurohypophysis of the pituitary. Double-label immunofluorescence revealed FSH and LH immunoreactivity co-localized in arginine vasotocin synthesizing preoptic neurons. Our results show that FSH and LH-producing cells have developmental origins in the brain as well as in the pituitary. In addition, we propose that the brain-derived gonadotropins may function as hypophysiotropic hormones that regulate pituitary cells and along with arginine vasotocin could act as neuromodulators of reproductive behaviors.

Age Factors↗