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PubMed1985

Altered follicular development in clomiphene citrate versus human menopausal gonadotropin-stimulated cycles for in vitro fertilization.

The pattern of periovulatory and luteal phase serum estradiol (E2) and progesterone (P) as well as follicular fluid (FF) E2, P, androgen, gonadotropin, and prolactin concentrations of eight women undergoing clomiphene citrate (CC)/human chorionic gonadotropin (hCG) stimulation and eight women undergoing human menopausal gonadotropin (hMG)/hCG stimulation of follicular development for the purpose of in vitro fertilization were compared. Ovulation was induced with either a 5-day course of CC (100 mg/day beginning on day 5 of the cycle) or an individualized hMG regimen, and laparoscopy was performed 36 hours after hCG administration. The length of the luteal phase was significantly longer (P less than 0.05) in the CC-treated group as compared with the hMG-treated group. The pattern of serum E2 levels differed significantly (P less than 0.01) in that E2 levels were lower in the early and midluteal phase in CC-stimulated cycles; in addition, a delayed second E2 peak was observed in the late luteal phase in these women. Serum P levels, however, were lower in the hMG-stimulated group. Analysis of FF hormone concentrations revealed significantly (P less than 0.05) higher concentrations of E2 and androsterone in the FF of hMG-treated patients. It is concluded that follicular development in CC-stimulated cycles differs markedly from that in hMG-stimulated cycles. These differences may reflect either an altered follicular maturational process or may represent a direct inhibitory effect of CC on follicular steroidogenesis.

Adult↗
PubMed1981

Hormonal correlates of follicular development in the human ovary.

This review summarizes recent studies pertaining to follicular development in the human ovary. Some of these studies were concerned with characterizing the steroidogenic capacity of the individual cell types of the follicle in relation to whether the follicle was healthy or atretic. Other studies covered in this review concern the oocyte and its hormonal environment both in vivo and in vitro, the effects of steroids and gonadotrophins on the steroidogenic potentials of follicle cells and also some endocrine and non-endocrine responses of thecal and granulosa cells after being separated and then recombined in vitro. The data are integrated in relation to the development of a follicle during the follicular phase of the menstrual cycle. The studies on the isolated cellular compartments of the follicle show that the biosynthetic and mitotic or developmental activities of granulosa cells and thecal tissues, and the behaviour of oocytes in vitro, all correlate with the hormonal microenvironments that they were previously exposed to in vivo rather than those in peripheral blood. The data suggest that the levels of steroid in follicular fluid and ovarian venous blood, collagen synthesis in the thecal tissue and mitotic activity of the granulosa cells are all dependent in part on a functional interaction between the thecal and the granulosa cells. It is concluded that the fate of a developing antral follicle centers around its ability to generate an oestrogen-enriched intrafollicular environment while simultaneously secreting both androgens and oestrogens into ovarian-venous blood.

Androstenedione↗
PubMed2002

Secretory pattern of inhibin A, inhibin B and inhibin pro-alpha C during induced follicular atresia and subsequent follicular development in the golden hamster (Mesocricetus auratus).

The changes in plasma concentrations of inhibins A, B and pro-alpha C were determined in the cyclic golden hamster during follicular atresia induced with antiserum against luteinizing hormone releasing hormone (LHRH-AS) at 1100 h on day 4 (day 1=day of ovulation). Follicular status in the ovary was also studied by determining the number of follicles ovulating in response to human chorionic gonadotrophin (hCG) injection. The time-courses of changes in plasma concentrations of inhibins A, B and pro-alpha C were different from each other during induced follicular atresia and subsequent follicular development. Plasma concentrations of inhibin A decreased to 58.6% of initial values by 24 h after LHRH-AS treatment, and then remained relatively low until at least 60 h later. Plasma concentrations of inhibin B decreased to 64.2% of the initial values by 18 h after LHRH-AS treatment and remained at basal values for 36 h, but increased abruptly to greater than initial values at 42 h after the treatment. Plasma concentrations of inhibin pro-alpha C increased at 6 and 12 h, decreased suddenly to 21.9% of the initial values by 24 h after LHRH-AS treatment, and then gradually increased until 60 h after LHRH-AS. The number of follicles responding to hCG decreased gradually between 0 and 30 h after LHRH-AS, when no ovulations were observed, and then gradually increased until 60 h. The changes in follicular ovulatory responses to hCG correlated with the plasma profile of inhibin A throughout the experiment. These results suggest that inhibin A is mainly secreted by large antral follicles. In contrast, during the subsequent follicular development, the plasma concentration of inhibin B increased earlier than that of inhibin A. These results suggest that inhibin B is secreted by small and large antral follicles. Plasma concentrations of inhibin pro-alpha C were high at a time when plasma concentrations of oestradiol-17 beta had already decreased, indicating that inhibin pro-alpha C is secreted not only from healthy follicles but also from early atretic antral follicles.

Animals↗
PubMed1993

Induction of follicular development in silver foxes (Vulpes vulpes) with equine chorionic gonadotrophin (eCG) and antibodies against eCG.

Experiments were conducted that demonstrated that 1000 iu equine chorionic gonadotrophin (eCG) was effective in induction of follicular development and ovulation in silver foxes during anoestrus. This treatment resulted in large, unovulated follicles; thus, trials in which the effects of eCG were reduced or abrogated by antibodies against eCG were carried out. Passive immunization against eCG on days 3 and 4 after eCG treatment interfered with subsequent follicular development and prevented ovulation. Treatment with eCG antibodies on days 5 or 7 after eCG treatment did not prevent ovulation and neutralization beginning on day 5 appeared to provide for the best ovulatory yield. The results suggest that combinations of eCG and anti-eCG antibody may provide a useful means of inducing ovarian activity in anoestrous foxes.

Anestrus↗
PubMed1989

Orchestrated expression of steroidogenic side-chain cleavage cytochrome P-450 during follicular development in the rat ovary.

Antibody to the mitochondrial cholesterol side-chain cleavage cytochrome P-450 (P-450scc) was used to study the expression of this key steroidogenic enzyme during follicular development. Immunofluorescence staining of tissue cryosections and isolated cells revealed unique and cell-specific patterns of P-450scc expressed in four cell types of the prepubertal rat ovary. Without hormonal treatment, the interstitial gland expressed ample amounts of P-450scc. Within 24 h after PMSG administration, theca interna acquired the cytochrome, and after an additional 24 h, the enzyme appeared also in granulosa cells. However, expression of P-450scc in granulosa cells was observed only in preovulatory follicles. This was in contrast to the theca interna cells which differentiated in various follicles unrelated to their stages of development. Cumulus cells were the last cell type to express P-450scc, occurring as late as 2-3 h before ovulation. These observations indicate that the concerted expression of P-450scc in the different ovarian cell types is a well-timed phenomenon which is precisely co-ordinated during follicular development.

Animals↗
PubMed1986

Cell-specific expression of immunoreactive cholesterol side-chain cleavage cytochrome P-450 during follicular development in the rat ovary.

Using a specific antiserum against rat cholesterol side-chain cleavage cytochrome P-450 (P-450scc), we examined the expression of this key steroidogenic enzyme during follicular development in PMSG-treated immature rats. The accumulation of the enzyme was monitored in ovary homogenates by quantitative immunodot blot assay, while expression of P-450scc in various cell types was visualized concomitantly by immunofluorescent staining of ovarian cryosections. Before PMSG treatment, no labeling of P-450scc could be observed in follicular granulosa cells. In contrast, steroidogenic cytochrome was markedly expressed in interstitial cells, part of theca interna cells, and hypertrophied theca of atretic follicles. As a result of PMSG treatment, the interstitial thecal cells promptly enriched their P-450scc content within 24 h, whereas the granulosa cells acquired the enzyme at a later time, between 30 and 48 h after hormone administration. After ovulation, many corpora lutea filled most of the ovarian volume, and the ovarian content of P-450scc was 47 times higher than that in control ovaries of untreated rats. In granulosa cell population of a single preovulatory follicle, a downward gradient of P-450scc expression was observed, starting high in the cells abutting the basal lamina and decreasing toward the cells lining the antrum. Cumulus cells failed to express P-450scc. Referring to the basal lamina, theca interna cells exhibited a reverse gradient of P-450scc expression, starting high in peripheral cells close to the theca externa layer and decreasing in cells located near the follicular basement membrane. Immunofluorescent labeling revealed a major difference between P-450scc expression in thecal cells compared to that in granulosa cells. While expression of P-450scc in granulosa cells was restricted exclusively to cells within preovulatory follicles, P-450scc labeling was observed throughout the ovary in thecal and interstitial cells associated with follicles at any phase of follicular maturation. Therefore, it may be proposed that the thecal and interstitial cells represent an all ovarian network which expresses its steroidogenic capacity at early stages of follicular maturation and thereby is able to supply androgens necessary for the follicular development.

Animals↗
PubMed1993

Suckling-induced inhibition of luteinizing hormone secretion and follicular development in the early postpartum sow.

The endocrine basis of lactational anestrus, the causes of reproductive dysfunction after early weaning, and the relationships among LH, FSH, and prolactin (PRL) secretion and follicular development were evaluated in sows weaned 6 h after farrowing (zero-weaned, n = 8) and in normally lactating sows (n = 9). An irregular, high-frequency episodic-type pattern of LH secretion was present in the early postpartum period, irrespective of treatment, and in a proportion of sows this pattern was associated with a marked elevation of baseline LH concentrations. This pattern of LH secretion was maintained in the zero-weaned sows but LH secretion was inhibited in lactating sows, resulting in a difference (p < 0.05) in mean plasma LH between groups 72-78 h postpartum. There were no differences in FSH between groups in any period of sampling. Variable but elevated plasma PRL was observed in suckled sows but declined (p < 0.05) to basal levels within 12 h of zero-weaning. Follicular development measured at laparotomy or slaughter 96 h postpartum was greater (p < 0.05) in zero-weaned than in control sows. The development of lactational anestrus in the sow therefore requires suckling-induced inhibition of LH secretion by 78 h postpartum. This inhibition of LH release does not appear to be causally related to short-term changes in PRL secretion.

Animals↗
PubMed1997

Lead-induced changes in ovarian follicular development and maturation in mice.

Lead, a potent reproductive toxicant in humans and experimental animals, was used to detect the morphological basis of ovarian toxicity in mice by counting the various stages of follicular development using different doses of lead acetate (0, 2, 4 or 8 mg/kg/d) for 60 d (5 d/wk) by oral gavage. Our results revealed that while small and medium follicles were significantly affected even at the lowest dose (2 mg), the large follicles were affected mostly at the highest dose. Atresia even in the medium follicles reflected the extent of damage caused by lead. These findings correlated well with increased blood lead levels. Therefore, lead seems to affect the follicular development and maturation, if mice are, exposed to sufficiently high concentrations of metal through the oral route.

Animals↗
PubMed1981

Monitoring of HMG-stimulated follicular development by real-time ultrasound.

Monitoring of human follicular development by real-time ultrasound during HMG-HCG treatment is presented. With the aid of ultrasound monitoring, the ovulation rate is raised to 94.3% (formerly 80% without ultrasound). Serious side effects such as ascites and/or hydrothorax did not occur in this study (1.2% without ultrasound controls). The pregnancy rate was 21/47 (44%) of all hormonally treated patients. By means of real-time sector scan examination, the growing follicle could be detected in 103/106 (97.3%) of HMG-HCG treated cycles. Thus real-time ultrasound examinations provide results comparable to those achieved mostly by time-consuming compound scan in demonstration of the growing follicle.

Anovulation↗
PubMed2005

Selection on predicted breeding value for milk production delays ovulation independently of changes in follicular development, milk production and body weight.

Two studies were conducted to investigate the effect of selection on predicted breeding value (PBV) for milk production, and its associated metabolic and endocrine milieu, on follicular development and ovulation in the postpartum period. A total of 71 cattle from lines selected to differ in their PBV were used in two consecutive years. In Study 1 the first ovulation and commencement of normal luteal function occurred significantly earlier in low (L) line cows than high (H) line cows. In Study 2 average daily milk production during the study period did not differ (P>0.10) between cows in either the H (=31.0+/-1.5kg/day) or L (=30.2+/-1.7kg/day) PBV lines although, 305 days milk production was significantly different (P<0.01; H=6880+/-164kg versus L=5795+/-317kg). As in Study 1, first ovulation postpartum in Study 2 occurred earlier (P<0.01) in the L (day 19) versus the H line (day 28). Circulating concentrations of glucose and insulin were significantly lower, whilst concentrations of GH and BOHB were higher in cows from the high PBV line. No differences in gonadotrophin concentrations were seen between lines. Both changes in body weight and patterns of follicle development did not differ between lines. By day 15 postpartum all cows had follicles of all three-size categories (small, medium-sized and large). Small (P<0.07) and medium-sized follicle numbers increased (P<0.01) with day postpartum. However, the inclusion of predicted changes in body weight as a covariate in the analysis, demonstrated that changes in number of small and medium-sized follicles were associated with changes in body weight. In conclusion, selection on PBV for milk production is associated with a longer interval from parturition to first ovulation, independent of changes in follicular development, milk production and body weight implicating other factor(s) associated with genetic selection.

Animals↗
PubMed1998

Recombinant human luteinizing hormone (LH) to support recombinant human follicle-stimulating hormone (FSH)-induced follicular development in LH- and FSH-deficient anovulatory women: a dose-finding study. The European Recombinant Human LH Study Group.

The efficacy of recombinant human LH (rhLH) for supporting human (rhFSH)-induced follicular development was investigated in hypogonadotropic hypogonadal women (WHO group I anovulation). Patients (n = 38) were randomized to receive rhLH (0, 25, 75, or 225 IU/day) in addition to a fixed dose of rhFSH (150 IU/day). rhLH was found 1) to promote dose-related increases in estradiol (E2) and androstenedione secretion by rhFSH-induced follicles, i.e. serum concentrations on the last day of FSH administration were 65 +/- 4, 195 +/- 94, 1392 +/- 585, and 2441 +/- 904 pmol/L for E2 and 3.6 +/- 0.9, 5.1 +/- 1.3, 6.4 +/- 1.3, and 6.7 +/- 1.3 nmol/L for androstenedione for patients treated with 0, 25, 75, and 225 IU rhLH, respectively; 2) to increase ovarian sensitivity to FSH, as demonstrated by the proportion of patients who developed follicles after the administration of a fixed dose of FSH, i.e. 1 of 8, 3 of 7, 7 of 9, and 8 of 10 in patients treated with 0, 25, 75, and 225 IU rhLH, respectively; and 3) to enhance the ability of these follicles to luteinize when exposed to hCG. A daily dose of 75 IU rhLH was effective in the majority of women in promoting optimal follicular development (defined as > or = 1 follicle > or = 17 mm; E2, > or = 400 pmol/L; midluteal phase progesterone, > or = 25 nmol/L) and maximal endometrial growth. A minority of patients may require up to 225 IU/day. rhLH, given sc at a dose up to 225 IU/day, was not immunogenic and was well tolerated.

Adult↗
PubMedDate not supplied

Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on serum inhibin concentrations and inhibin immunostaining during follicular development in female Sprague-Dawley rats.

Intact and hypophysectomized immature rats were pretreated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; 0 or 32 microg/kg p.o.) and sacrificed throughout synchronized follicular development (0, 12, 24, 48, and 72 h after equine chorionic gonadotropin, eCG). TCDD administration to intact rats resulted in a premature elevation of serum FSH and LH by 12 h post-eCG. In intact rats pretreated with TCDD, the intensity of ovarian immunoreactivity for inhibin and the number of ovarian follicles staining for inhibin in midsaggital ovarian sections were decreased at the time of eCG administration (24 h post-TCDD) in comparison to controls. However, this decreased ovarian staining for inhibin was not associated with alterations in serum inhibin concentrations. Serum inhibin was suppressed in TCDD-treated rats when compared to intact controls only at 24 h post-eCG. Hypophysectomized animals exhibited no effect of TCDD on serum inhibin at any timepoint but did have decreased estradiol concentrations during follicular development. In summary, TCDD reduced serum concentrations of inhibin after the premature increases in FSH and LH suggesting that inhibin is not important in the initial elevation of FSH following exposure to TCDD.

Animals↗
PubMed1992

Regulation of estrous cycle in hysterectomized albino rats by activation of follicular development.

Wistar strain albino rats were hysterectomized and the estrous cycle was compared with sham operated controls. Duration of estrous cycle in hysterectomized rats increased markedly with significant delay in the luteal phase and this was correlated to the inhibited follicular development of ovary. When these rats were treated with PGF2 alpha and PMSG and subjected to physical exercises, the estrous cycle was synchronised and the ovaries of such animals had active follicular development. Thus the deranged operation of sexual cycle in hysterectomized rats was regulated through physical exercises.

Animals↗
PubMed1986

Effect of LHRH immunoneutralization on follicular development, the LH surge and luteal function in the stumptailed macaque monkey (Macaca arctoides).

A dose of 100 microliter of a potent ovine LHRH gamma globulin inhibited ovulation in the cyclic rat when administered at 12:00 h on the day of pro-oestrus. A dose of 10 ml of the preparation was administered i.v. to female stumptailed macaques to achieve circulating antibody titres 3-4-fold higher than in the rat. In an ovariectomized macaque, this caused a marked fall in serum concentrations of LH to less than 10% of pretreatment values and also a significant, though less pronounced, fall in FSH. Six monkeys were treated with the LHRH gamma globulin during the mid-late follicular phase of the cycle. In 2 monkeys in which serum oestradiol concentrations were less than 100 pg/ml at the time of antibody administration, the rising oestradiol levels were abruptly suppressed and the normal mid-cycle LH surge failed to occur. Serum concentrations of LH and FSH declined to low levels for 8-10 days after which time normal follicular development occurred. In the remaining 4 monkeys in which follicular development was more advanced as indicated by serum oestradiol concentrations of greater than 100 pg/ml, the antibodies induced either a transient decline or had no effect on the rising serum concentration of oestradiol. An LH/FSH surge followed by a rise in serum progesterone occurred in these macaques. When the antibodies were administered to a further 6 macaques, which had also been treated with oestradiol benzoate during the early follicular phase to induce an LH surge, the neutralization of LHRH again failed to block the surge even when the dose of antibody was increased to 20 ml. The results show that LHRH antibodies were unable to block the LH surge in the macaque. They contrast with results obtained with LHRH immunoneutralization in the sheep, rat, hamster, mouse and bird and suggest that the ability of oestrogen to induce an LH surge by acting directly on the LHRH-primed anterior pituitary gland is more dominant in the primate.

Animals↗
PubMed1993

[Follicular development patterns in infertile women with biphasic basal body temperature].

Seventy-one cases of infertile women with both normal menstrual cycle and biphasic BBT were studied with ultrasonography, laparoscopy, hormonal assay and endometrial histology. Signs for follicular development and ovulation were divided into four types: (1) normal ovulation in 12 cases; (2) ovulation of small follicle in 21 cases; (3) luteinized unruptured follicle in 15 cases; (4) small luteinized follicle in 23 cases. Mean serum progesterone levels in the luteal phase were within normal limits in all cases. Secretory endometrium accounted for 77.46%. Proliferative or hyperplastic endometrium accounted for 22.54%. The Authors conclude that the criteria of biphasic BBT, P levels and endometrial histology are not reliable enough for determine the cause of female infertility women. In this study the rate of salpingitis: and the rate of aberration of follicular development and chronic anovulation was 7.04%, 83.10% respectively. The latter played an important role in causing female infertility.

Adult↗
PubMed1997

Up-regulation of urokinase plasminogen activator messenger ribonucleic acid and protein in hen granulosa cells by transforming growth factor alpha in vitro during follicular development.

The aim of the present study was to examine the regulatory role of transforming growth factor alpha (TGF alpha) on urokinase plasminogen activator (uPA) gene expression and protein levels in hen granulosa cells from different stages of ovarian follicular development in vitro. Granulosa cells from the first (F1), the second and third (F2-3), and the fourth, fifth, and sixth (F4-6) largest preovulatory follicles were cultured for 21 h in the absence and presence of TGF alpha (10 ng/ml). The uPA mRNA abundance and protein content were determined by Northern and Western blot analysis, respectively. Cell-associated and secreted PA activity was measured by a fibrinolysis assay and characterized by zymography. Hen granulosa cells produce a uPA with a molecular mass of about 35 kDa and a transcript size of approximately 2.5 kb. Basal uPA mRNA abundance, protein content, and activity were highest in granulosa cells from F4-6 follicles and decreased with follicular maturation. Granulosa cell uPA mRNA levels, protein content, and activity were increased in the presence of TGF alpha, reaching maximal levels in granulosa cells from less mature follicles, although the percentage of stimulation was higher in cells from late stages of follicular development. These findings clearly demonstrate specific expression of uPA in proliferatively active granulosa cells and responsiveness of uPA to TGF alpha at both transcriptional and translational levels. They support the concept that PA of the urokinase type plays an important role in extracellular matrix remodeling during TGF alpha-induced granulosa cell proliferation and ovarian follicular growth.

Animals↗
PubMed2002

[Revisiting the role of LH in follicular development].

During the last decade, two pivotal events widened the gap between the hormonal dynamics of ovarian stimulation and that of the menstrual cycle. First, the profound and routine suppression of endogenous gonadotropins by GnRH analogues used in ovarian stimulation pressed us to recreate the hormonal environment necessary for adequate follicular maturation and steroidogenesis. Second, drugs with reduced or null LH activity became available, based on the hypothesis that FSH action was sufficient to follicular development and maturation irrespective of residual endogenous gonadotropin levels. Today, there is a renewed interest in the possible role of LH on follicular development, in an effort to mimic the hormonal events of the menstrual cycle to optimize ovarian stimulation outcome.

Female↗
PubMed2001

Short-term administration of antivascular endothelial growth factor antibody in the late follicular phase delays follicular development in the rhesus monkey.

Indirect evidence in the nonhuman primate and human suggests that angiogenesis and regulators of angiogenesis such as vascular endothelial growth factor (VEGF) may play an active role in cyclic folliculogenesis. Indeed, the follicle selected for maturation and ovulation possesses a denser microvascular network, and VEGF messenger ribonucleic acid and its protein have been identified in granulosa cells of the developing follicle during the mid- and late follicular phases, with a more intense signal in the mature follicle. The objective of this study was to obtain direct evidence in the nonhuman primate for an active role of VEGF in follicular growth and maturation by studying the effect of VEGF-blocking antibodies in this process. After documenting two normal ovulatory cycles, female rhesus monkeys (n = 7) received iv injections of anti-VEGF antibodies (0.5 mg) twice on successive days in the late follicular phase. Three monkeys also received nonspecific goat IgG (0.5 mg) twice on successive days in the late follicular phase. Daily measurements of estradiol, progesterone, LH, and FSH were obtained during the two control cycles, the anti-VEGF treatment and posttreatment cycles, and the IgG treatment cycle. Anti-VEGF antibody administration significantly lengthened the follicular phase in six of seven monkeys to 17.8 +/- 1.7 vs. 10.0 +/- 0.7 and 9.8 +/- 0.6 in control cycles and 10.7 +/- 0.3 days (mean +/- SE) in IgG-treated cycles. The expected late follicular phase rise in estradiol, as documented in the control cycles (day 0, 96.1 +/- 6.0; day 1, 125.5 +/- 20.0; day 2, 165.5 +/- 24.9; day 3, 183.8 +/- 11.0 pg/mL), was interrupted by anti-VEGF antibody treatment (99.3 +/- 5.0, day 0, preinjection control) to 63.3 +/- 12.2 (day 1), 48.5 +/- 8.7 (day 2), and 57.6 +/- 9.0 (day 3). Mean FSH levels were significantly increased by day 2 of anti-VEGF antibody treatment. After a variable delay, estradiol concentrations increased to reach a preovulatory peak in all anti-VEGF-treated animals, followed by ovulation, normal luteal function, and a normal posttreatment cycle. The data clearly demonstrate that short-term inhibition of angiogenesis with an anti-VEGF-blocking antibody during the later growth phase of the dominant follicle interferes with normal follicular development. Persistence of estradiol secretion and delayed resumption of its rise also suggest recovery of the follicle. We conclude that the angiogenic regulator VEGF is a crucial component in the process of follicular growth in the primate.

Animals↗