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PubMed2005

Microsomal prostaglandin E synthase-1 (mPGES-1) is the primary form of PGES expressed by the primate periovulatory follicle.

BACKGROUND: Prostaglandin E2 (PGE2) has been identified as the key ovulatory PG in the primate follicle. Follicular PGE2 levels increase just before the expected time of ovulation, suggesting that the midcycle LH surge induces the expression of enzymes involved in PGE2 synthesis. METHODS: To identify the specific form(s) of prostaglandin E synthase (PGES) expressed by the primate periovulatory follicle, we examined granulosa and theca cell expression of the three microsomal (m) and cytosolic (c) forms of PGES (mPGES-1, mPGES-2 and cPGES) identified to date. Monkey granulosa cells and whole monkey ovaries were obtained from animals receiving exogenous gonadotropins to stimulate multiple follicular development; monkeys then received an ovulatory dose of HCG to initiate periovulatory events. RESULTS: Expression of mPGES-1 mRNA and protein by granulosa cells of periovulatory follicles increased in response to HCG administration, peaking just before the expected time of ovulation. Immunocytochemistry showed that mPGES-1 protein was present in both granulosa and theca cells of monkey periovulatory follicles. Monkey granulosa cells also expressed mPGES-2 and cPGES mRNA, but mRNA levels did not change in response to HCG administration. Isolated monkey theca cells expressed both mPGES-1 and cyclooxygenase-2 mRNA, and produced PGE2 in vitro. Human granulosa-lutein cells obtained from women undergoing treatment for infertility expressed mRNAs for mPGES-1, mPGES-2 and cPGES. CONCLUSIONS: These data indicate that mPGES-1 is a gonadotropin-regulated PG synthesis enzyme expressed by granulosa cells of primate periovulatory follicles and suggest that mPGES-1 may be the primary PGES responsible for the increased follicular PGE2 levels necessary for primate ovulation.

Animals↗
PubMed1991

Oxytocin stimulates progesterone production by bovine granulosa cells isolated before, but not after, the luteinizing hormone surge.

Oxytocin and its mRNA have been detected in bovine granulosa cells, but the function of follicular oxytocin is not well understood. We have shown previously that oxytocin exerts a specific, dose-dependent, stimulatory effect on progesterone secretion by granulosa, but not theca cells isolated from bovine preovulatory follicles obtained 48 h after the initiation of luteolysis. The objective of the present study was to characterize the development of granulosa cell responsiveness to oxytocin during the follicular phase. Granulosa cells and theca interna were isolated form preovulatory follicles early in the follicular phase (24 h after the initiation of luteolysis) or after the luteinizing hormone (LH) surge and cultured in defined medium for 5 days with or without oxytocin and in the presence or absence of gonadotropins. Granulosa, but not theca cells obtained before the LH surge increased progesterone production 3.3-fold in response to oxytocin. However, late in the follicular phase, after the LH surge, granulosa cells did not respond to oxytocin (or to follicle-stimulating hormone (FSH) or LH). These findings suggest that the LH surge (1) stimulates granulosa cells to maximal progesterone secretion, so that they cannot be further stimulated, (2) abolishes the responsiveness of granulosa cells to oxytocin, or (3) stimulates granulosa cells to increase oxytocin production, so that exogenous oxytocin has no additional effect.

Animals↗
PubMed1991

Possible role for arachidonic acid in the control of steroidogenesis in hen theca.

Studies were conducted to evaluate if arachidonic acid (C20:4) could function as a second messenger within theca cells from the second largest preovulatory (F2) follicle from the ovary of the domestic hen. Arachidonic acid stimulated basal progesterone and androstenedione production, but inhibited LH-induced androstenedione production. The stimulatory effects of arachidonic acid were not altered by either cyclooxygenase or lipoxygenase pathway inhibitors (indomethacin and nordihydroguaiaretic acid, respectively), but were blocked by agents that prevented mobilization and/or efflux of calcium (TMB-8 and verapamil). The inhibitory effects of arachidonic acid on LH-stimulated steroidogenesis were determined to occur both prior and subsequent to cAMP formation. Fifty and 100 microM arachidonic acid attenuated LH- (10 ng) and forskolin- (0.2 microM) induced cAMP levels, and decreased androstenedione and estradiol production following treatment with 8-bromo-cAMP. Phospholipase A2 (PLA2) and the calcium ionophore, A23187, stimulated the release of 3H from theca cells prelabeled with [3H]arachidonic acid, and both PLA2 and the closely related fatty acid, eicosatrienoic acid (C20:3), could replicate the inhibitory effects of arachidonic acid on LH-stimulated androstenedione production. Finally, neither indomethacin nor nordihydroguaiaretic acid blocked the inhibitory effects of arachidonic acid on LH-promoted androstenedione production. We conclude that arachidonic acid can be released within theca cells in response to physiologic (PLA2) and pharmacologic agents (A23187), and accordingly, that it may act directly as a second messenger to modulate both basal and LH-stimulated steroid production.

Androstenedione↗
PubMed2001

Immunohistochemical localization of taurine in the rat ovary, oviduct, and uterus.

The distribution of the amino acid taurine in the female reproductive organs has not been previously analyzed in detail. The aim of this study was to determine taurine localization in the rat ovary, oviduct, and uterus by immunohistochemical methods. Taurine was localized in the ovarian surface epithelium. The granulosa cells and oocytes of primordial follicles were immunonegative. In primary and antral follicles, taurine was found mainly in theca cells and oocytes, whereas the zona pellucida, antrum, and most granulosa cells were unstained. However, taurine immunoreactivity in theca cells and oocytes decreased during follicular atresia. During corpora lutea development, the number of immunopositive theca lutein cells increased as these cells invaded the granulosa-derived region. Therefore, most luteal cells from the mature corpora lutea were stained. In the regressing corpora lutea, however, taurine staining in luteal cells decreased. In the fimbriae, infundibulum, and uterotubal junction, taurine was localized in most epithelial cells. In the ampullar and isthmic segments, taurine was found in the cilia of most ciliated cells and in the apical cytoplasm of some non-ciliated cells. In the uterus, most epithelial cells were immunopositive during diestrus and metestrus, whereas most of them were immunonegative during estrus and proestrus. Moreover, taurine immunoreactivity in the oviduct and uterus decreased with pregnancy. (J Histochem Cytochem 49:1133-1142, 2001)

Animals↗
PubMed1992

Human intraovarian interleukin-1 (IL-1) system: highly compartmentalized and hormonally dependent regulation of the genes encoding IL-1, its receptor, and its receptor antagonist.

To delineate the scope of the human intraovarian IL-1 system we used a solution hybridization/RNase protection assay to test for expression of the genes encoding IL-1, its type I receptor (IL-1R), and its receptor antagonist (IL-1RA). IL-1 transcripts were not detected in whole ovarian material from days 4 or 12 of an unstimulated menstrual cycle but transcripts (IL-1 beta much greater than IL-11 alpha) were detected in preovulatory follicular aspirates from gonadotropin-stimulated cycles. Concurrently obtained peripheral monocytes did not contain IL-1 beta transcripts but macrophage-depleted follicular aspirates did, thus implicating the granulosa cells as the site of IL-1 expression. IL-1R transcripts were detected in RNA from whole ovaries and follicular aspirates but not in RNA from peripheral monocytes. IL-1RA transcripts were detected in whole ovarian material as well as in macrophage-free follicular aspirates. Cultured human granulosa and theca cells did not contain mRNA for IL-1 beta or IL-1RA but did contain mRNA for IL-1R. Treatment of cell cultures with forskolin (25 microM) induced IL-1 beta transcripts in granulosa but not theca cells. Forskolin also increased the basal levels of IL-1R transcripts in both granulosa and theca cells but did not induce IL-RA transcripts in either cell type. Taken together, these findings reveal the existence of a complete, highly compartmentalized, hormonally dependent intraovarian IL-1 system replete with ligands, receptor, and receptor antagonist.

Adult↗
PubMed1989

Ovarian renin production in vitro and in vivo: characterization and clinical correlation.

The purpose of this study was to examine the in vitro production of prorenin and active renin by human theca cells and to examine the clinical significance of this production by correlating prorenin and active renin levels with oocyte maturity in follicular fluid samples. Human theca cell cultures were established and were found to produce both prorenin as well as active renin. Androstenedione levels (126 +/- 28 pg/500,000 cells/24-hr incubation) correlated with prorenin levels (8.5 +/- 1.1 ng angiotensin I per milliliter per hour (AI/ml/hr) in culture supernatant (r = 0.61, P less than 0.05). Active renin levels in follicular fluid were higher in stimulated versus spontaneous cycles (359 +/- 67 versus 126 +/- 37 ng AI/ml/hr, P less than 0.05). Renin substrate levels were similar in follicular fluid and in the peripheral serum (1,610 +/- 216 versus 2,160 +/- 490 ng/ml) in spontaneous cycles. Follicular fluid prorenin and active renin did not correlate with oocyte maturity or with steroid levels. The authors conclude that ovarian theca cells produce renin in vitro. However, renin production does not correlate with oocyte maturity or follicular fluid steroids in vivo.

Androstenedione↗
PubMed1999

Proliferation and differentiation of rat theca-interstitial cells: comparison of effects induced by platelet-derived growth factor and insulin-like growth factor-I.

This study was designed to evaluate mechanisms regulating proliferation of steroidogenically active and steroidogenically inactive theca-interstitial (T-I) cells, and, specifically, to evaluate the effects of platelet-derived growth factor (PDGF) and insulin-like growth factor-I (IGF-I). T-I cells obtained from immature Sprague-Dawley rats were cultured in chemically defined media. Proliferation was assayed by thymidine incorporation and cell counting. Steroidogenically active cells were identified by the presence of 3beta-hydroxysteroid dehydrogenase activity. Flow cytometry facilitated separation of dividing cells (in S and G2/M phases of the cell cycle) from nondividing cells (in G0 and G1 phases of the cell cycle). PDGF alone (0.1-1 nM) produced a dose-dependent increase in DNA synthesis by up to 136%. IGF-I alone (10 nM) increased DNA synthesis by 56%. In the presence of both IGF-I (10 nM) and PDGF (0.1-1 nM), DNA synthesis increased by 108-214%. PDGF (1 nM) increased the total number of T-I cells by 43%; this effect was due to an increase in the number of steroidogenically inactive cells (47%). In contrast, the stimulatory effect of IGF-I (10 nM) was predominantly due to an increase in the number of steroidogenically active cells (163%). Separation of dividing cells from nondividing cells was accomplished with the aid of flow cytometry. In the absence of growth factors, the proportion of steroidogenically active cells was 35% lower among proliferating than resting cells. PDGF (1 nM) decreased the proportion of steroidogenically active cells among both proliferating and resting cells (by 43% and 16%, respectively). In contrast, IGF-I (10 nM) increased the proportion of steroidogenically active cells among proliferating cells by 56%. These findings indicate that differentiated/steroidogenically active cells divide; furthermore, PDGF and IGF-I may selectively stimulate proliferation of individual subpopulations of T-I cells, thereby providing a mechanism for development of structural and steroidogenically active components of the T-I compartment.

Animals↗
PubMed2003

Follicle-restricted compartmentalization of transforming growth factor beta superfamily ligands in the feline ovary.

Ovarian follicular development, follicle selection, and the process of ovulation remain poorly understood in most species. Throughout reproductive life, follicle fate is balanced between growth and apoptosis. These opposing forces are controlled by numerous endocrine, paracrine, and autocrine factors, including the ligands represented by the transforming growth factor beta (TGFbeta) superfamily. TGFbeta, activin, inhibin, bone morphometric protein (BMP), and growth differentiation factor 9 (GDF-9) are present in the ovary of many animals; however, no comprehensive analysis of the localization of each ligand or its receptors and intracellular signaling molecules during folliculogenesis has been done. The domestic cat is an ideal model for studying ovarian follicle dynamics due to an abundance of all follicle populations, including primordial stage, and the amount of readily available tissue following routine animal spaying. Additionally, knowledge of the factors involved in feline follicular development could make an important impact on in vitro maturation/in vitro fertilization (IVM/IVF) success for endangered feline species. Thus, the presence and position of TGFbeta superfamily members within the feline ovary have been evaluated in all stages of follicular development by immunolocalization. The cat inhibin alpha subunit protein is present in all follicle stages but increases in intensity within the mural granulosa cells in large antral follicles. The inhibin betaA and betaB subunit proteins, in addition to the activin type I (ActRIB) and activin type II receptor (ActRIIB), are produced in primordial and primary follicle granulosa cells. Additionally, inhibin betaA subunit is detected in the theca cells from secondary through large antral follicle size classes. GDF-9 is restricted to the oocyte of preantral and antral follicles, whereas the type II BMP receptor (BMP-RII) protein is predominantly localized to primordial- and primary-stage follicles. TGFbeta1, 2, and 3 ligand immunoreactivity is observed in both small and large follicles, whereas the TGFbeta type II receptor (TGFbeta RII) is detected in the oocyte and granulosa cells of antral follicles. The intracellular signaling proteins Smad2 and Smad4 are present in the granulosa cell cytoplasm of all follicle size classes. Smad3 is detected in the granulosa cell nucleus, the oocyte, and the theca cell nucleus of all follicle size classes. These data suggest that the complete activin signal transduction pathway is present in small follicles and that large follicles primarily produce the inhibins. Our data also suggest that TGFbeta ligands and receptors are colocalized to large antral follicles. Taken together, the ligands, receptors, and signaling proteins for the TGFbeta superfamily are present at distinct points throughout feline folliculogenesis, suggesting discrete roles for each of these ligands during follicle maturation.

Activins↗
PubMed2003

[Enlarged ovary in a mare: review of the literature and a case report].

Mares regularly have an enlarged ovary. The main causes are haematomas, anovulatory follicles, abscesses, and neoplasia. The granulosa-theca-cell tumour is by far the most common neoplasia of the ovary (about 97%) and accounts for 2.5% of all equine tumours. In this article the differential diagnosis of an enlarged ovary and the background of granulosa-theca cell tumours are reviewed. A case is described of a mare with a very large granulosa-theca cell tumour in the left ovary, which was discovered 1 month after delivery of a healthy foal. This case is special not only because the tumour was enormous (diameter 60 cm) but also because the contralateral ovary was functional and there were no behavioural changes. The fact that a haematoma had been found 2 years earlier made the diagnosis even more difficult.

Animals↗
PubMed1999

Relaxin-like factor (RLF): a new specific marker for Leydig cells in the ovary.

Relaxin-like factor (RLF), also known as the Leydig cell insulin-like factor (Ley-I-L), is a novel member of the insulin-IGF-relaxin family of hormones and growth factors that has recently been shown to be strongly expressed in testicular Leydig cells. Expression of the RLF peptide in the human ovary and in ovarian tumors has not been studied. In the present study, the expression of the RLF peptide in the human ovary was investigated by immunohistochemistry using a specific antibody raised against human RLF. By this method, RLF was found to be expressed in hilus (Leydig) cells and theca interna cells but absent in granulosa cells, ovarian stromal cells, and surface epithelium. RLF expression was also observed in the corpus luteum, although at a lower level than in theca cells. Thirty-seven sex cord-stromal tumors and five cases of hilar Leydig cell hyperplasia were also investigated for RLF expression. RLF was found to be strongly expressed in hilar Leydig cell hyperplasia and sex cord-stromal tumors with a component of Leydig or luteinized cells. Of the analyzed theca cell tumors, two displayed a diffuse staining pattern. As expected, RLF was not expressed in granulosa cell tumors. In conclusion, RLF appears to be a useful marker for Leydig cells in the human ovary and may be a diagnostic supplement in hyperplasias and tumors derived therefrom.

Biomarkers, Tumor↗
PubMed1990

Immunohistochemical localization of epidermal growth factor-like activity in the hamster ovary with a polyclonal antibody.

A polyclonal antibody to murine epidermal growth factor (EGF) was generated in rabbits and characterized by RIA, Western blots, and dot blotting. The antibody detected as little as 0.01 ng of mouse EGF in dot blots at 1:100,000 dilution and 5 pg of EGF in RIA at 1:50,000 dilution; it did not cross-react with transforming growth factor-alpha, insulin-like growth factor, or fibroblast growth factor. Ovarian EGF content peaked (17 +/- 2 pg/nonluteal ovary) on Day 1 (estrus as determined by copious vaginal discharge) and declined by DAy 3 as measured by RIA of immunoaffinity-purified ovarian extract. Frozen sections of hamster ovaries were stained immunohistochemically for EGF using a Zymed kit. Intense red staining specific for EGF was localized only in granulosa cells of small (1-2 layers of granulosa cells) and medium (3-6 layers of granulosa cells) preantral follicles; moderate staining was observed in the granulosa and theca cells of small antral follicles. Staining intensity faded in granulosa and theca cells of large antral follicles, especially on Day 4 (proestrus) and disappeared in pyknotic granulosa cells of atretic follicles. Follicular EGF staining peaked on Days 1 and 2 and thereafter declined to low levels. On Day 2, oocytes of the primordial follicles showed distinct coloration. Sections of Day 2 ovary incubated with preneutralized antibody or normal rabbit IgG did not show any coloration. For intact hamsters, 10 micrograms of follicle-stimulating hormone (FSH), twice daily for Days 1 and 2, intensified EGF staining in granulosa cells compared with corresponding untreated Day 3 hamsters, whereas similar treatment with luteinizing hormone for 2 days expanded the interstitium with localized staining of interstitial cells only around follicles with 2 and 3 layers of granulosa cells and lacking theca. Hypophysectomy for 13 days resulted in almost complete absence of EGF-specific staining in the remaining nonatretic follicles; however, exogenous FSH (5 micrograms, twice daily) for 2 days dramatically increased staining intensity associated with newly developed follicles. Luteinizing hormone (0.4 micrograms, twice daily) for 2 days, however, induced significant development of only the interstitium with increased staining of small preantral follicles. These results provide strong evidence for the presence of EGF-like activity in hamster ovarian follicles and suggest that its expression is controlled by gonadotropins, especially FSH.

Animals↗
PubMed1989

Localization of gonadotropin binding sites in human ovarian neoplasms.

The binding of human luteinizing hormone and human follicle-stimulating hormone to ovarian tumor biopsy specimens from 29 patients was analyzed. The binding sites for human luteinizing hormone were demonstrated in one tumor of epithelial origin (mucinous cystadenoma) and in one of sex cord-stromal origin (theca cell tumor). The binding sites for human follicle-stimulating hormone were found in three tumors of epithelial origin (serous cystadenoma and mucinous cystadenoma) and in two of sex cord-stromal origin (theca cell tumor and theca-granulosa cell tumor). The surface-binding autoradiographic study revealed that the binding sites for gonadotropins were localized in the stromal tissue. The results suggest that gonadotropic hormones may play a role in the growth and differentiation of a certain type of human ovarian neoplasms.

Adolescent↗
PubMed2004

Proliferation of ovarian theca-interstitial cells is modulated by antioxidants and oxidative stress.

BACKGROUND: Maintenance of ovarian homeostasis requires precise regulation of proliferation of thecal- interstitial (T-I) cells. Recent evidence indicates that oxidative stress and antioxidants modulate proliferation of various tissues under both physiological and pathological conditions. This study evaluated the effects of oxidative stress and antioxidants on T-I proliferation. METHODS: Rat T-I cells were cultured in serum-free medium and proliferation was assessed by determination of DNA synthesis using the thymidine incorporation assay, by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay and by direct counting of steroidogenically active cells and steroidogenically inactive cells. RESULTS: Antioxidants and reactive oxygen scavengers induced a dose-dependent decrease of T-I proliferation. Vitamin E succinate was inhibitory at 10-100 micro mol/l, ebselen was inhibitory at 0.3-30 micro mol/l, and superoxide dismutase was inhibitory at 300-1000 IU/ml. In contrast, oxidative stress resulted in a biphasic effect. Modest oxidative stress induced by 1 mmol/l hypoxanthine and xanthine oxidase (3-30 micro U/ml) stimulated proliferation of T-I cells, while greater oxidative stress induced by xanthine oxidase (1 mU/ml) profoundly inhibited proliferation. Direct cell counting demonstrated comparable effects on steroidogenically active and inactive cells. CONCLUSIONS: Reactive oxygen species may play a role in the regulation of growth of ovarian mesenchyme. Under pathological conditions, such as those encountered in polycystic ovary syndrome, excessive oxidative stress and depletion of antioxidants may contribute to ovarian mesenchymal hyperplasia.

Animals↗
PubMed1985

Evidence for a granulosa cell site of dihydrostestosterone metabolism in the adult rat ovary.

The ovarian enzyme 3 alpha-hydroxysteroid dehydrogenase (3 alpha-HSD) converts dihydrotestosterone (DHT) to 5 alpha-androstan-3 alpha,17 beta-diol (3 alpha-diol), a reduced androgen that does not bind to the granulosa cell androgen receptor. To determine the relative contribution of the granulosa cells to total ovarian 3 alpha-HSD activity, adult rats treated with either medroxyprogesterone acetate (MPA) or vehicle underwent ovarian microdissection. 3 alpha-Hydroxysteroid dehydrogenase is primarily located in excised follicles and corpora lutea, and is inhibited in the follicles but not corpora lutea by MPA (P less than 0.05). Elimination of healthy granulosa cells while maintaining healthy theca cells by irradiation of the exteriorized ovaries with 6000 rads resulted in a marked reduction in 3 alpha-HSD to 19% of control levels on a per-organ basis (P less than 0.01). The granulosa cell is the major ovarian site for 3 alpha-hydroxylation of ring A-reduced C19 steroids in the adult rat.

3-Hydroxysteroid Dehydrogenases↗
PubMed1994

An immunohistochemical study of the vascularization of the human Graafian follicle.

The wall of the largest Graafian follicle or corpus luteum was biopsied in 22 patients at laparoscopy. Both granulosa and theca cells were contained in 18 samples. These samples were classified as pre-luteinizing hormone (LH) surge (n = 3), LH surge (n = 3), early luteal (n = 3), mid-luteal (n = 4), late luteal (n = 3) and menstrual (n = 2). A double-staining immunohistochemical protocol was used to demonstrate proliferating endothelial cells: mouse-anti-rat-proliferating cell nuclear antigen, for proliferating cells; mouse-anti-human-CD34 antibody for endothelial cells. The percentage of endothelial cells proliferating (proliferation index) and the area of tissue occupied by endothelial cells (areal fraction) were determined for granulosa and theca layers. Intra- and inter-slide coefficients of variation were < 15%. The granulosa layer was avascular until the LH surge subsided. Maximum vascularization was achieved by the mid-luteal phase. The theca endothelial cell proliferation index was constant from pre-LH surge to mid-luteal phases. The mean theca endothelial cell proliferation index for these phases was significantly greater than for the late luteal and menstrual phases. From first appearance in the granulosa layer, endothelial cells had the same proliferation index as the theca endothelial cells, the proliferation index decreasing significantly in both after the mid-luteal phase (P = 0.018). It is concluded that endothelial cell proliferation is unchanged throughout the follicular, early and mid-luteal phases, decreasing significantly in the late luteal phase. By contrast, endothelial cell invasion of the membrane granulosa, presumably in response to a chemotactic stimulus, occurs after the LH surge has subsided.

Antigens, CD↗
PubMed2004

Gene expression and protein localisation for activin-A, follistatin and activin receptors in goat ovaries.

We studied the protein and mRNA expression of activin-A, follistatin and activin receptors in goat ovaries to find evidence of their possible role in ovarian activity, particularly in the various stages of follicle development. Ovaries of cyclic goats were collected and then either fixed in paraformaldehyde for immunohistochemical localisation of activin-A, follistatin, activin receptors IIA/B (ActR-IIA/B) and IA (ActR-IA) proteins or used to obtain samples to demonstrate mRNA expression of activin-A (betaA subunit), follistatin, ActR-IIA, -IIB, -IA and -IB, using RT-PCR. For this latter goal, primordial, primary and secondary follicles were isolated mechanically, washed to remove the stromal cells and then used for RT-PCR. In addition, oocytes, cumulus, mural granulosa and theca cells from small (<3 mm) and large (3-6 mm) antral follicles, luteal cells and surface epithelium were collected to study mRNA expression. Activin-A and follistatin proteins were found in oocytes of all follicle classes, granulosa cells from the primary follicle stage onwards, theca cells of antral follicles, corpora lutea and ovarian surface epithelium. In antral follicles, these proteins were detected both in cumulus and mural granulosa cells. ActR-IIA/B protein was found at the same follicular sites, and also in granulosa cells of primordial follicles onward. The localisation of ActR-IA corresponded with that of ActR-IIA/B, but the former protein was absent in the theca of large antral follicles. The mRNAs for activin-A (betaA subunit), follistatin, and ActR-IIA, -IIB, -IA and -IB were detected at all follicular and cellular types studied, except that ActR-IIB was not found in follicles that had not developed an antrum yet. In conclusion, in goat ovaries, transcripts of activin-A (betaA subunit), its receptors and its binding protein follistatin are expressed and their proteins formed at all follicular stages and in corpora lutea. These findings indicate a role of activin-A in the local regulatory system during the entire follicular development and during luteal activity.

Activin Receptors↗
PubMed2000

Roles of KIT and KIT LIGAND in ovarian function.

Evidence from mouse mutants indicates that the Kit gene encoding KIT, a receptor present on the oocyte and theca cells, and the Mgf gene encoding KIT LIGAND, the ligand of KIT, are important regulators of oogenesis and folliculogenesis. Recently, in vitro cultures of fetal gonads, of follicles and of oocytes have identified specific targets for the KIT-KIT LIGAND interaction. In fetal gonads, an anti-apoptotic effect of KIT-KIT LIGAND interactions on primordial germ cells, oogonia and oocytes has been demonstrated. In postnatal ovaries, the initiation of follicular growth from the primordial pool and progression beyond the primary follicle stage appear to involve KIT-KIT LIGAND interactions. During early folliculogenesis, KIT together with KIT LIGAND controls oocyte growth and theca cell differentiation, and protects preantral follicles from apoptosis. Formation of an antral cavity requires a functional KIT-KIT LIGAND system. In large antral follicles, the KIT-KIT LIGAND interaction modulates the ability of the oocyte to undergo cytoplasmic maturation and helps to maximize thecal androgen output. Hence, many steps of oogenesis and folliculogenesis appear to be, at least in part, controlled by paracrine interactions between these two proteins.

Animals↗
PubMed2005

Proliferation and apoptosis in ovarian stromal hyperplasia and hyperthecosis.

The aim of our study was to investigate proliferation and apoptosis in ovarian stromal hyperplasia and hyperthecosis in reproductive women with and without polycystic ovarian disease. We have studied 104 patients with a histological diagnosis of ovarian stromal hyperthecosis and stromal hyperplasia. Paraffin sections were stained by hematoxylin-eosin, von Gieson and immunohistochemistry for Bcl-2 (anti-apoptotic protein) and Ki-67 antigen (proliferation marker). We assessed the number of Bcl-2-positive and Ki-67-positive cells. The patients were divided into 4 groups: group 1 -- 33 patients with polycystic ovarian disease and coexistent stromal hyperthecosis, group 2 -- 28 patients with polycystic ovarian disease and coexistent stromal hyperplasia, group 3 -- 24 patients with ovarian stromal hyperthecosis, group 4-19 patients with ovarian stromal hyperplasia. The results suggest that in ovarian stromal hyperthecosis coexistent with polycystic ovarian disease luteinized stromal cells show high proliferation activity and resistance to apoptosis, and internal and external theca cells show resistance to apoptosis. In ovarian stromal hyperplasia coexistent with polycystic ovarian disease, hyperplastic stromal cells show high proliferation activity and resistance to apoptosis. Proliferation activity is also increased in vascular endothelial and smooth muscle cells. Internal and external theca cells show resistance to apoptosis. In ovarian stromal hyperthecosis without polycystic ovarian disease, luteinized stromal cells show high proliferation activity and resistance to apoptosis. In ovarian stromal hyperplasia without polycystic ovarian disease, hyperplastic stromal cells show high proliferation activity and potential susceptibility to apoptosis. Proliferation activity is also increased in vascular endothelial and smooth muscle cells. These characteristics of proliferation and apoptosis have meaning in pathogenesis of ovarian stromal hyperthecosis and stromal hyperplasia with and without polycystic ovarian disease.

Apoptosis↗