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PubMed1996

Expression of CCAAT enhancer binding protein-alpha (C/EBP alpha) in the rat ovary: implications for follicular development and ovulation.

The development of follicles from the antral to the preovulatory stage in the mammalian ovary involves both proliferation and differentiation of cells. These processes are coordinated by endocrine, paracrine, and autocrine factors in a time- and cell-specific pattern. Each stage of development is characterized by expression of specific genes the products of which are involved in different cellular processes, e.g., signal transduction (cAMP-dependent protein kinases), steroidogenesis (cytochrome P450 enzymes). At the nuclear level, the signaling pathway from external stimuli converges to modify the mechanisms of transcription factors. One such factor, CCAAT enhancer binding protein-alpha (C/EBPalpha), participates in differentiation processes of several organs, e.g., liver, adipose tissue, and gut. We have previously demonstrated that C/EBPalpha is expressed in rat ovarian follicles in a cell-, time-, and hormone-specific manner. This increase in granulosa cells was concomitant with the more differentiated phenotype. The aim of the present study was to explore the function of C/EBPalpha in the rat ovary. To achieve this, the expression of C/EBPalpha in follicular cells was attenuated in vivo by the local administration of antisense oligonucleotides (AS) into the ovarian bursa, i.e., the sac-like structure surrounding the ovary of immature rats. This administration resulted in an impaired response to subsequent injections of exogenous gonadotropins (PMSG, hCG) with an attenuated expression of C/EBPalpha protein and finally a decreased ovulation rate. Furthermore, the morphology of the AS-treated ovary was altered with large, oocyte-containing follicles at a time when ovaries exposed to sense (S) oligonucleotides demonstrated newly formed corpora lutea. AS also affected the expression of the proto-oncogene c-myc, which was elevated by this treatment. The administration of S was without effects. Thus, C/EBPalpha seems to be a necessary factor for follicular development in the rat ovary.

Animals↗
PubMed2002

The role of LH and FSH in ovarian androgen secretion and ovarian follicular development: clinical studies in a patient with isolated FSH deficiency and multicystic ovaries.

Inactivating mutations have proven to be instructive in elucidating the role of FSH in human ovarian function. We performed a detailed reproductive endocrine evaluation of a patient with inactivating mutations in the FSH beta-subunit gene who was hypo-estrogenic and had LH excess. The patient underwent a pelvic ultrasound and overnight frequent blood sampling followed by a human chorionic gonadotrophin (HCG) stimulation test. One month later she received human recombinant FSH, followed 24 h later by a second HCG stimulation test. Despite a mean LH serum concentration and LH pulse characteristics typical for polycystic ovaries (PCOS), baseline and dexamethasone-suppressed free testosterone were low-normal. The administration of HCG led to minimal stimulation of 17-hydroxyprogesterone and androgens. The patient had multicystic ovaries containing follicles 3-5 mm in diameter and responded to FSH with prompt increases in estradiol and inhibin B. There were no clinical or laboratory consequences of LH excess in this FSH-deficient woman. These findings support the hypothesis that excessive LH stimulation alone does not cause ovarian hyperandrogenism. We also found that follicular development was present in the absence of FSH. These antral follicles had apparently developed normally, since estradiol and inhibin B increased promptly after FSH administration.

17-alpha-Hydroxyprogesterone↗
PubMed2001

High FSH:LH ratio and low LH levels in basal cycle day 3: impact on follicular development and IVF outcome.

PURPOSE: To examine the impact of low basal cycle day 3 serum LH levels or a high FSH:LH ratio on IVF results. METHODS: A homogeneous group of patients was analyzed as identified by normal basal cycle of follicle stimulating hormone (FSH), Luteinizing hormone (LH), and estradiol (E2) levels. High responders (high LH:FSH ratio) and low responders (high FSH or E2 levels, and women > or = 42 years of age) were excluded from analysis. Only cycles stimulated with a combination of a GnRHa (luteal suppression) and pure FSH were studied. RESULTS: Patients with low basal LH levels (< 3 mIU/mL) did not differ significantly from controls in terms of response to controlled ovarian hyperstimulation but there was a clear trend toward poorer implantation and clinical pregnancy rates. On the other hand, patients with a high FSH:LH ratio (> 3) had significantly fewer mature oocytes aspirated, and lower implantation and clinical pregnancy rates than patients with gonadotropin ratio < or = 3. These negative effects were evident in the presence of normal basal FSH levels and after adequate matching of female's age and number of embryos transferred. CONCLUSIONS: These studies highlight a negative impact of a basal cycle high FSH:LH ratio (and possibly low LH levels) on follicular development and oocyte quality in these patients subjected to pituitary down-regulation followed by pure FSH administration. A high FSH:LH ratio may be therefore used as an early biomarker of poor ovarian response.

Adult↗
PubMed1988

Induction of luteal regression in the marmoset monkey (Callithrix jacchus) by a gonadotrophin-releasing hormone antagonist and the effects on subsequent follicular development.

Doses of 100 or 200 micrograms of a novel GnRH antagonist ([N-acetyl-D beta Na11-D-pCl-Phe2-D-Phe3-D-Arg6-Phe7-Arg8-D-Ala10]NH2 GnRH) (4 animals/dose) were administered on Days 10/11 of the luteal phase and induced a marked suppression of circulating bioactive LH and progesterone concentrations within 1 day of treatment (P less than 0.01). Thereafter, progesterone concentrations remained low or undetectable until after the next ovulation. Similar results were obtained when 200 micrograms antagonist were given on Days 5/6 of the luteal phase (N = 4). The interval from injection of antagonist (200 micrograms but not 100 micrograms) to ovulation (based on a rise in progesterone above 10 ng/ml) was significantly longer than that from prostaglandin-induced luteal regression to ovulation in control cycles (N = 4/treatment) (range, 13-15 days after antagonist vs 8-10 days after prostaglandin, P less than 0.01). This delay of 4-5 days was equivalent to the duration for which LH concentrations were significantly suppressed by 200 micrograms antagonist when administered to ovariectomized animals (N = 3). Corpus luteum function during the cycle after GnRH antagonist treatment appeared normal according to the pattern of circulating progesterone. These results show that corpus luteum function and preovulatory follicular development in the marmoset monkey are dependent on pituitary gonadotrophin secretion.

Animals↗
PubMed1994

The effects of gonadotrophin-releasing hormone agonist on follicular development in patients with polycystic ovary syndrome in an in-vitro fertilization and embryo transfer programme.

The aim of the study was to evaluate ovarian response to gonadotrophin stimulation, with and without premedication with gonadotrophin-releasing hormone (GnRH) agonist, in patients with polycystic ovary syndrome. In all, 40 women included in the in-vitro fertilization/embryo transfer programme were divided into two groups. In the first group, buserelin, 500 micrograms/day s.c., was given until pituitary desensitization was achieved. Ovarian stimulation was performed by the combination of GnRH agonist and human menopausal gonadotrophin (HMG). The second group was treated using a conventional HMG and human chorionic gonadotrophin (HCG) protocol. Desensitization was achieved in 15.2 +/- 6.3 days (mean +/- SD) and the luteinizing hormone:follicle stimulating hormone ratio decreased from 2.84 +/- 1.54 to 0.60 +/- 0.35. Comparing the duration of stimulation, the number and size of all observed and aspirated follicles, oocytes recovered and fertilized and the number of embryos replaced, no statistically significant differences were found between the groups. The average oestradiol concentration on the day of HCG administration was lower in the group treated with premedication (P < 0.05). These data suggest that short pre-treatment with GnRH agonist can temporarily correct endocrine abnormalities of polycystic ovary syndrome but do not change the ovarian response to gonadotrophin stimulation and multiple follicular development.

Adult↗
PubMed2006

Similar ovulation rates, but different follicular development with highly purified menotrophin compared with recombinant FSH in WHO Group II anovulatory infertility: a randomized controlled study.

BACKGROUND: The contribution of the LH activity in menotrophin preparations for ovulation induction has been investigated in small trials conducted versus FSH preparations. The objective of this study was to demonstrate non-inferiority of highly purified urinary menotrophin (HP-HMG) versus recombinant FSH (rFSH) with respect to the primary outcome measure, ovulation rate. METHODS: This was a randomized, open-label, assessor-blind, multinational study. Women with anovulatory infertility WHO Group II and resistant to clomiphene citrate were randomized (computer-generated list) to stimulation with HP-HMG (n=91) or rFSH (n=93) using a low-dose step-up protocol. RESULTS: The ovulation rate was 85.7% with HP-HMG and 85.5% with rFSH (per-protocol population), and non-inferiority was demonstrated. Significantly fewer intermediate-sized follicles were observed in the HP-HMG group (P<0.05). The singleton live birth rate was comparable between the two groups. The frequency of ovarian hyperstimulation syndrome and/or cancellation due to excessive response was 2.2% with HP-HMG and 9.8% with rFSH (P=0.058). CONCLUSIONS: Stimulation with HP-HMG is associated with ovulation rates at least as good as a rFSH in anovulatory WHO Group II women. LH activity modifies follicular development so that fewer intermediate-sized follicles develop. This could have a positive impact on the safety of ovulation induction protocols.

Adolescent↗
PubMed2005

Dietary galactose inhibits GDF-9 mediated follicular development in the rat ovary.

Clinical evidence suggests an association between galactosemia and premature ovarian failure, but the mechanism is still not fully understood. Growth differentiation factor-9 (GDF-9) is thought to be an obligatory growth factor during the gonadotropin-independent phase of folliculogenesis. The objective of this study was to examine the effects of galactose on initiation of folliculogenesis in the peripubertal interval and the connection between galactose toxicity and GDF-9 expression in the ovary. After immature Long-Evans rats (n = 10) were fed a diet consisting of 20% galactose for 19 days, whole body, ovary and uterine weights were measured. Serum estradiol and progesterone concentrations were measured by radioimmunoassay. Ovarian follicles were counted by morphometric analysis and GDF-9 expression was investigated by immunohistochemistry and immunoblot assay. Galactose treatment did not affect the onset of puberty as marked by the time of vaginal opening. The galactose diet significantly decreased the number of healthy growing follicles. The results of immunoblot assay showed that both bands corresponding to propeptide and mature forms of GDF-9 decreased with the galactose diet about 90 and 70%, respectively. The results of immunohistochemical staining showed that the GDF-9 positive follicle number and the ratio of GDF-9 positive to GDF negative (primordial/non-growing) follicles significantly decreased with this high galactose diet. The present study suggests that a high galactose diet inhibits follicular development, possibly through down-regulation of GDF-9 in the rat ovary, implying that GDF-9 may be involved in galactose-related ovarian toxicity.

Animals↗
PubMed1995

Disturbance of follicular development and endocrine reactions induced by the antiovulatory effective progesterone antagonist Onapristone.

The present study was undertaken to investigate whether inhibition of ovulation, which is known to occur after treatment with progesterone antagonists, is due to the effect of high levels of prolactin. Therefore, rats with 4-day cycles were treated with the antiprogestin, Onapristone (ON), once daily starting on the evening of estrus. It was detected that the profile of peripheral prolactin levels during the treatment with ON was not remarkably different from that found in the controls. Furthermore, bromocriptine, a prolactin antagonist, was not able to reverse the antiovulatory potency of ON. It is concluded that the antiovulatory effect of ON might not be related to changes in the level of prolactin. Nevertheless, prolactin levels remained high after the preovulatory surge. Thus, we cannot exclude the possibility that PRL plays a role in the induction of anovulatory cycles observed during long term treatment. In animals treated for the length of one cycle we found that the preovulatory LH surge decreased but it remains questionable whether this contributes to the inhibition of ovulation by ON. Interestingly, basal LH, androgen and estrogen levels were elevated. Accordingly, we favour the idea that LH stimulates the theca interstitial cells to produce excessive amounts of androgens which may be aromatized into estrogens. These high levels of androgens and estrogens may contribute to the antiovulatory mechanism of ON by disturbing physiological follicular development. In fact, a morphometrical analysis revealed an increase in the volume density of late tertiary follicles. The increased progesterone levels may also be related to high basal LH levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Androstenedione↗
PubMed1986

Comparison between clomiphene plus pulsatile human menopausal gonadotrophin and clomiphene plus pulsatile follicle stimulating hormone in induction of multiple follicular development in women.

Eighteen normally cycling women with tubal infertility undergoing in-vitro fertilization and embryo transfer were treated with clomiphene only (nine cycles), clomiphene plus human menopausal gonadotrophin (HMG) (18 cycles) and clomiphene plus follicle-stimulating hormone (FSH) (12 cycles). Clomiphene was given from day 2 to 6 (150 mg daily). HMG and FSH were injected s.c. in a pulsatile manner via a pump (28 IU every 3 h). Plasma FSH and oestradiol levels and the number of follicles greater than or equal to 16 mm in diameter were similar in the clomiphene/HMG and the clomiphene/FSH cycles, but significantly higher than in the clomiphene-only cycles. In contrast, luteinizing hormone and progesterone levels during the treatment did not differ significantly among the three regimens. Twelve of the 18 women were treated with clomiphene/HMG in one cycle and clomiphene/FSH in another and eight of them with clomiphene only in a third cycle (a total of 32 cycles). In the clomiphene/HMG cycle seven of these 12 women (58%) had plasma FSH levels during treatment similar to those in the clomiphene/FSH cycle and six of them (86%) had the same number of follicles in both cycles. A significant, but not very strong correlation was found between FSH treatment levels and the number of follicles greater than or equal to 16 mm when all 32 cycles were combined (r = 0.40). It is suggested that pulsatile HMG and FSH in combination with clomiphene are in general equally effective in inducing multiple follicular development in normal women. However, individual responses show great variability.

Clomiphene↗
PubMed2005

Role of nitric oxide in ovarian follicular development and egg production in Japanese quail (Coturnix coturnix japonica).

Role of nitric oxide (NO) in regulating the reproductive functions at hypothalamo-hypophysealovarian axis in Japanese quail was studied. In first experiment, metabolites of NO, i.e. nitrite and nitrate (NO2 and NO3) were estimated together in hypothalamus, serum and ovarian follicles of good and poor layers. In the second experiment, different NO modulators such as L-arginine (L-Arg), sodium nitroprusside (SNP) and N(G)-nitro-L-arginine methyl ester, HCl (L-NAME) were administered to the birds. In the first experiment, significantly higher (P < 0.01) NO2 and NO3 levels in serum, hypothalamus and largest (F1) ovarian follicles were observed in good layers as compared to poor layers. Higher (P < 0.05) NO2 and NO3 concentration was observed in F1 follicles than smaller follicles (F2) only in good layers. The NO2 and NO3 concentration was significantly reduced (P < 0.05) in post ovulatory follicles (POFs) in comparison to F1 and F2 follicles. In the second experiment, the serum NO2 and NO3 concentrations were higher (P < 0.05) in the SNP, lower (P < 0.05) in the L-Name group and unchanged in the L-Arg treated group in comparison to control group. compared to control, L-Arg and SNP increased (P < 0.05) the hypothalamic NO2 and NO3 concentration where as L-NAME reduced (P < 0.05) these levels. The NO2 and NO3 concentration was increased (P < 0.05) as the follicle size increased and it was significantly reduced (P < 0.05) in POFs. The higher (P < 0.05) follicular NO2 and NO3 concentration was observed in L-Arg group in comparison to control group. Egg production was also found to be higher (P < 0.05) in L-Arg group whereas it was not different (P > 0.05) in SNP and L-NAME treated groups. The yolk weight and yolk to albumin ratio was reduced (P < 0.05) in L-NAME group in comparison to control group. It may be concluded from the present study that NO plays a key role in regulating follicular development, ovulatory mechanisms and egg production in Japanese quail.

Animals↗
PubMed1997

[Participation of the follicular fluid in follicular development, oocyte maturation and spermatic function].

Follicular fluid (FF) is of great importance in Assisted Procreation Programmes, because it constitutes the micro-environment of the follicle that regulates the development of the oocyte and participates in the capacitation of the spermatozoa. The biochemical composition of FF is influenced by the state of follicle maturation and reciprocally the content of the fluid predicts the success of the subsequent follicular maturation and pregnancy. In most of the species the high concentrations of estradiol are common in the follicles of intermediate maturity, the progesterone in the mature ones and the androgens in the atresics ones. Estradiol concentration is associated with the fertilizing capacity of the oocytes and its metabolites stimulate the progesterone production. Moreover, the FF regulates the action of the gonadotrophins, because it contains factors that help the union of these with its receptor. The FF contributes providing factors that inhibit and stimulate the meiosis. It contains factors that stimulates oocyte maturation, or that block the ability of the cortical granules to modify the components of the pellucid zone. The exposition of spermatozoons with this fluid helps the acrosomal reaction, the spermatic motility and the ovum penetration.

Chorionic Gonadotropin↗
PubMed2001

Effects of nitric oxide on steroidogenesis in porcine granulosa cells during different stages of follicular development.

BACKGROUND: We have previously demonstrated that nitric oxide (NO) inhibits steroidogenesis via a cGMP-independent process, by inhibiting P450 aromatase activity in porcine granulosa cells (PGCs) derived from medium-sized (3--5 mm) ovarian follicles (M-PGC). OBJECTIVE: To determine whether the NO/NO synthase (NOS) system exerts any significant effects on steroidogenesis in PGCs derived from small follicles (<3 mm) (S-PGC) in comparison with those derived from medium follicles. DESIGN AND METHODS: PGCs, namely S-PGC and M-PGC, were incubated with the NO donor, NOC18, and a competitive blocker of NOS, N(3)-monomethyl-l-arginine (LNMMA), either alone or in the presence of FSH (200 ng/ml) or hCG (5 IU/ml). RESULTS: NOC18 significantly (P<0.01--0.001) suppressed basal (unstimulated) and gonadotropin-stimulated estradiol (E2) release from both S-PGC and M-PGC in a 2-h culture. NOC18 significantly (P<0.01--0.001) decreased basal and gonadotropin-stimulated progesterone release from S-PGC, but not from M-PGC. In addition, NOC18 significantly (P<0.05--0.001) inhibited aromatase activity in S-PGC. LNMMA had a significantly (P<0.01--0.001) stimulatory effect on the basal release of E2 and progesterone from M-PGC; however, it had no significant effect on basal steroidogenesis in S-PGC in a 24-h culture. In the presence of gonadotropin, LNMMA significantly (P<0.01--0.001) stimulated the release of E2 and progesterone from both S- and M-PGC, and this stimulatory effect was weaker in S-PGC than in M-PGC. These results demonstrate that NO inhibits E2 secretion by directly inhibiting the aromatase activity in S-PGC, as in M-PGC. It has been shown that the NO system suppresses the differentiation of S-PGC; however, the extent of suppression decreased with the progression of follicular growth. In addition, the activity of NOS in S-PGC was weaker than that in M-PGC. CONCLUSION: We strongly suggest that the NO/NOS system in PGC regulates steroidogenesis differently during different phase of follicular development.

Animals↗
PubMed1987

Tissue distribution and hormonal regulation of messenger ribonucleic acid for regulatory and catalytic subunits of adenosine 3',5'-monophosphate-dependent protein kinases during ovarian follicular development and luteinization in the rat.

cDNA probes specific for the regulatory (R) subunits [RII51; (mol wt, 51,000) and RI (mol wt, 49,000)] and a catalytic (C alpha) subunit of cAMP-dependent protein kinases were used to analyze the hormonal regulation, tissue distribution, and content of mRNAs for these kinase subunits in the rat ovary. Filter hybridization assays demonstrated that mRNA specific for RII51 increased in both thecal and granulosa cells of preovulatory (PO) follicles, then declined precipitously (less than 10-fold) in both cell types within 7 h after an ovulatory (10-IU) dose of hCG and remained low in corpora lutea. Dose-response studies showed that doses of FSH greater than 2 micrograms were required to increase RII51 mRNA in granulosa cells of hypophysectomized (H) rats, whereas doses of 0.5-1.0 micrograms were effective in granulosa cells of H estradiol-treated (HE) rats. At all doses (0.5-50 micrograms) of FSH administered, RII51 mRNA was 4 times higher in granulosa cells of HE rats than in H rats. Solution hybridization assays demonstrated that the concentration of RII51 mRNA increased 6-fold from 20 molecules/granulosa cell in H rats to 120 molecules/cell in H rats treated with estradiol and FSH (HEF). Transcription assays using nuclei of granulosa cells demonstrated further that the 5- to 10-fold increases in RII51 mRNA content in estradiol-/FSH-induced granulosa cells was associated with increased transcription of the RII51 gene. In thecal cells of small antral (SA), PO, and luteinizing follicles, changes in the content of mRNA for RI and C alpha kinase subunits showed a pattern similar to that for RII51. However, in granulosa cells, mRNA specific for RI and C alpha was highest in SA follicles, declined in PO follicles, and remained unchanged during luteinization. The content of mRNA for RI (45-70 molecules/cell) and C alpha (10 molecules/cell) also changed less than 2-fold in granulosa cells of H, HE, and HEF rats. In summary, these results indicate that the content of RII51 mRNA is hormonally regulated in both thecal cells and granulosa cells during follicular development and luteinization. Low concentrations of gonadotropins increase RII51 mRNA, whereas an ovulatory dose of hCG causes mRNA for RII51 to decrease rapidly. In granulosa cells, induction of mRNA for RII51, but not that for RI and C alpha is induced by the actions of estradiol and FSH, and involves increased transcription of the RII51 gene.

Animals↗
PubMed1995

Intracrine role of progesterone in follicle-stimulating hormone- and cyclic adenosine 3',5'-monophosphate-induced fibronectin production and deposition by chicken granulosa cells: influence of follicular development.

The role of progesterone in FSH- and 8-bromo-cAMP (8-Br-cAMP)-induced fibronectin production by chicken ovarian granulosa cells was examined. Granulosa cells isolated from the third largest (F3; developing; 15-20 mm in diameter) preovulatory follicle and a pool of immature small yellow follicles (SYF; 6-8 mm in diameter) were incubated in serum-free medium 199, and the total amount of fibronectin produced (deposited, secreted into the medium, and associated with cells) was measured by enzyme-linked immunosorbent assay. Unstimulated F3 cells deposited greater amounts of fibronectin than unstimulated SYF cells. FSH or 8-Br-cAMP significantly increased fibronectin deposition. Similarly, both agents increased the quantity of fibronectin secreted into the medium and that associated with cells. The magnitude of FSH- and 8-Br-cAMP-enhanced fibronectin deposition or secretion into medium by SYF cells was greater than that by F3 cells. Cyanoketone (an inhibitor of progesterone synthesis) significantly suppressed basal fibronectin production by F3 cells, but not that by SYF cells. Cyanoketone completely blocked FSH- or 8-Br-cAMP-induced fibronectin production by F3 cells, but caused only a modest inhibition (nonsignificant) of agonist-induced fibronectin production by SYF cells. Exogenous progesterone completely reversed the inhibitory effects of cyanoketone on agonist-induced fibronectin production. The nondegradable synthetic progestin R5020 also reversed the inhibitory effects of cyanoketone on agonist-induced fibronectin production. The antiprogestin, ZK 98.299, inhibited basal and FSH-stimulated fibronectin production. The data demonstrate that FSH- and cAMP-stimulated fibronectin production by chicken granulosa cells is dependent (at least in part) on de novo progesterone synthesis. Furthermore, they indicate that fibronectin production and deposition by these cells are stimulated by progesterone, perhaps in an intracrine/autocrine manner, and that the role of progesterone increases with advancing stages of follicular development.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2000

Effect of basal lamina on progesterone production by chicken granulosa cells in vitro--influence of follicular development.

Experiments were conducted in vitro to study the regulation of progesterone production in chicken granulosa cells by homologous basal lamina isolated from preovulatory follicles of chicken ovary. The majority of components of the basal lamina (90-95% by weight) were solubilized with guanidine-HCl (and designated fraction 1); the remaining components were solubilized with beta-mercaptoethanol containing guanidine-HCl (and designated fraction 2). The ability of fraction 1 to regulate progesterone production in granulosa cells obtained from the largest (F(1), mature), third largest (F(3), growing), fifth to seventh largest (F(5-7), growing) follicles and a pool of small yellow follicles (SYF, immature) of chicken ovary was assessed. Granulosa cells isolated from SYF follicles were in the least differentiated (undifferentiated) and those obtained from F(1) follicles were in the most differentiated state. The ability of fraction 1 to regulate progesterone production by chicken granulosa cells was influenced both by the state of cell differentiation and the form of the matrix material (whether solid or liquid). When fraction 1 was added as liquid to the incubation mixture, it promoted progesterone production by granulosa cells at all stages of differentiation; however, it caused a greater relative increase in the amount of progesterone produced by undifferentiated (SYF) and differentiating (F(3)) granulosa cells than by differentiated (F(1)) ones. In the presence of the liquid-form of fraction 1, luteinizing hormone (LH) stimulated progesterone production in differentiated (F(1)) and differentiating (F(5-7)) granulosa cells. Similarly, follicle-stimulating hormone (FSH) stimulated progesterone production by differentiating (F(3)) and undifferentiated (SYF) granulosa cells in the presence of the liquid-form of fraction 1 protein. In culture wells that had been pre-coated with fraction 1 (solid-form), progesterone production by less differentiated (SYF, F(5-7)) granulosa cells was enhanced, whereas progesterone production by differentiated (F(1)) cells was reduced. The solid-form of fraction 1 augmented LH-stimulated progesterone production by less differentiated (F(5-7)) granulosa cells however, it attenuated LH-induced progesterone production in differentiated (F(1)) cells. FSH-promoted progesterone production in granulosa cells from immature follicles (SYF) was augmented by solid-form of fraction 1 whereas the effect of FSH on cells obtained from older follicle (F(3)) was suppressed by solid-form of fraction 1. In experiments in which gonadotropin action was attenuated by solid-form of fraction 1, the amount of progesterone produced in the presence of maximally inhibiting concentrations of fraction 1 protein was greater than control values (no fraction 1, no gonadotropin). These results show that basal lamina of the ovarian follicle can regulate progesterone production by granulosa cells. The data demonstrate that the interactions between the components of basal lamina and LH or FSH on granulosa cell function were dependent on the stage of follicular development and were influenced by the form of the matrix material. It is concluded that the basal lamina of the chicken ovarian follicle is biologically active and regulates granulosa cell function.

Animals↗
PubMed2004

Estimation of the follicle-stimulating hormone (FSH) threshold for initiating the final stages of follicular development in women with elevated FSH levels in the early follicular phase.

OBJECTIVE: To test the hypothesis that the follicle-stimulating hormone (FSH) threshold in patients with elevated FSH levels in the early follicular phase (EFP) is higher than in controls. DESIGN: Pilot study. SETTING: Academic hospital. PATIENT(S): Six patients with elevated EFP FSH (>10 IU/L) and 13 controls. INTERVENTION(S): Treatment with a GnRH agonist in the midluteal phase before IV administration of recombinant FSH was started in an ultra-low-dose step-up protocol. The FSH threshold was determined by the mean of FSH levels of the above threshold value and the below threshold value. MAIN OUTCOME MEASURE(S): Follicle-stimulating hormone threshold, FSH screening value, E(2), number of follicles. RESULT(S): The FSH threshold in the elevated EFP FSH group was 6.75 IU/L and was significantly higher than the FSH threshold of the controls (4.65 IU/L). The FSH screening value on day 3 was 12.0 IU/L in the patient group and 5.0 IU/L in the controls. Estradiol was significantly lower on the day that the largest follicle was 18 mm in the elevated EFP FSH group compared with controls (277 vs. 491 pmol/L, respectively). On the day of hCG administration, the number of smaller (10-13 mm) follicles was equal but the number of larger (>14 mm) follicles was higher in the control group compared with the elevated FSH group. In the control group, the basal FSH levels correlated highly with the FSH threshold levels (r = 0.8), but in the patients with elevated EFP FSH this correlation was absent. CONCLUSION(S): In normal women, basal FSH day 3 values represent the ovarian threshold for FSH. In women with elevated day 3 FSH, the FSH threshold is higher but not as high as basal FSH values. We postulate that the FSH threshold in patients with elevated EFP FSH is higher because of intraovarian factors. Basal FSH overshoots the threshold, probably because of the limited feedback by the ovary.

Chorionic Gonadotropin↗
PubMed2000

Follicular development in vitro.

There has been tremendous interest in recent years in the culture of oocytes and follicles. Although much of the research using follicle culture aims to increase understanding of the regulation of follicle development, an important goal has been to develop a method that will eventually allow maturation of human oocytes from the primordial follicle to the mature Graafian stage. We are still some way from this at present, although it has now been achieved in the mouse. In this article, we consider various methods of follicle culture for primordial, preantral, and antral follicles. In vitro development of primordial follicles has used primarily whole ovaries or ovarian fragments as a source of follicles. Culture of later stages of follicle development uses mainly isolated follicular units, either whole (with an intact basement membrane and, in some cases, attached thecal cells) or nonintact (oocyte-somatic cell complexes, which may or may not have remnants of basement membranes and/or thecal cells attached).

Animals↗
PubMed2005

Acceleration of follicular development by administration of vascular endothelial growth factor in cycling female rats.

To address the role of follicular angiogenesis in the determination of ovulatory follicles and the effects of different vascular endothelial growth factor (VEGF) isoforms on follicular angiogenesis and development, mature female rats were treated with an angiogenic inhibitor (TNP-470), and also with VEGF 120 or 164 at different dosages (0.4, 0.8, 4.0 or 8.0 microg/kg body weight) for 3 days during the estrous cycle. Ovarian follicular angiogenesis, the population of large follicles and ovulation were examined. VEGF 120 (0.8 microg/kg) and 164 (8.0 microg/kg) treatments stimulated follicular angiogenesis in the theca interna layer, while TNP-470 treatment showed severe depression of follicular angiogenesis, and completely inhibited ovulation. After administration of VEGF 120 or 164, the number of healthy preovulatory follicles and ovulated oocytes increased significantly, concomitantly with a decrease in the number of atretic preovulatory follicles. The oocytes ovulated had normal fertilizability and developed to term with the same litter size as in the control rats. Our findings suggest that follicular angiogenesis may be a determinant of follicular development during the periovulatory phase, and that VEGF isoforms may play different important roles in regulating follicular angiogenesis.

Angiogenesis Inhibitors↗