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PubMed2006

Effects of metformin on bovine granulosa cells steroidogenesis: possible involvement of adenosine 5' monophosphate-activated protein kinase (AMPK).

In mammals, IGFs are important for the proliferation and steroidogenesis of ovarian cells. Metformin is an insulin sensitizer molecule used for the treatment of the infertility of women with polycystic ovary syndrome. It is, however, unclear whether metformin acts on ovarian cells. Adenosine 5' monophosphate-activated protein kinase (AMPK) is involved in metformin action in various cell types. We investigated the effects of metformin on bovine granulosa cell steroidogenesis in response to IGF1 and FSH, and studied AMPK in bovine ovaries. In granulosa cells from small follicles, metformin (10 mM) reduced production of both progesterone and estradiol and decreased the abundance of HSD3B, CYP11A1, and STAR proteins in presence or absence of FSH (10(-8) M) and IGF1 (10(-8) M). In cows, the different subunits of AMPK are expressed in various ovarian cells including granulosa and theca cells, corpus luteum, and oocytes. In bovine granulosa cells from small follicles, metformin, like AICAR (1 mM) a pharmaceutical activator of AMPK, increased phosphorylation of both Thr172 of AMPK alpha and Ser 79 of ACACA (Acetyl-CoA Carboxylase). Both metformin and AICAR treatment reduced progesterone and estradiol secretion in presence or absence of FSH and IGF1. Metformin decreased phosphorylation levels of MAPK3/MAPK1 and MAPK14 in a dose- and time-dependent manner. The adenovirus-mediated production of dominant negative AMPK abolished the effects of metformin on secretion of progesterone and estradiol and on MAPK3/MAPK1 phosphorylation but not on MAPK14 phosphorylation. Thus, in bovine granulosa cells, metformin decreases steroidogenesis and MAPK3/MAPK1 phosphorylation through AMPK activation.

AMP-Activated Protein Kinases↗
PubMed1997

Identification and localization of deoxyribonuclease I in the rat ovary.

Our objective was to identify the endonuclease responsible for DNA degradation in the ovary and determine its localization relative to the developmental state of ovarian follicles. Immature rats were treated with diethylstilbestrol (DES; DES group), DES + eCG (eCG group) or DES + eCG + hCG (hCG group). Nuclei of the eCG and hCG but not the DES group contained a 32/34-kDA DNase I-like endonuclease activity that was Ca2+/Mg(2+)-dependent, stimulated by Mn2+, optimal at pH 7, and identified by anti-DNase I antibody. G-actin, Zn2+, dithiothreitol, aurintricarboxylic acid, and sodium aurothiomalate, but not iodoacetic acid, inhibited the activity. Addition of eCG nuclear protein extracts to nuclei from the DES group induced oligonucleosomal DNA fragmentation, which could be prevented by pretreatment of the extracts with anti-DNase I antibody. DNase I was immunolocalized in nuclei of healthy luteal cells, antral follicle granulosa cells, oocytes of preantral follicles, atretic preantral follicles, and testicular spermatogonia, but was not observed in granulosa cells of preantral follicles, theca cells, antral follicle oocytes, or testicular spermatocytes. Nuclear extracts of rat kidney, liver, and spleen, and bovine, chicken, and human ovaries displayed DNase I-like activity. These results suggest that an endonuclease indistinguishable from DNase I is responsible for ovarian apoptotic DNA degradation.

Animals↗
PubMed1998

Immunohistochemical distribution of follistatin in dominant and subordinate follicles and the corpus luteum of cattle.

The study was done to quantitatively characterize the distribution of follistatin in ovarian follicles and corpora lutea at specific stages of development. Transrectal ultrasonography was used to monitor the growth of individually identified follicles from 2 days before ovulation until the day of ovariectomy on Day 3 of wave 1 (n = 8), Day 6 of wave 1 (n = 6), Day 1 of wave 2 (n = 6), or after onset of proestrus, at least 17 days postovulation (n = 7). Days of ovariectomy represent the growing, early-static, late-static, and regressing phases of the dominant follicle of wave 1, respectively. Subordinate (n = 24), preselection (n = 15), and preovulatory (n = 6) follicles and corpora lutea (n = 31) were also analyzed. Follistatin was localized using immunohistochemical labeling of paraffin sections, and relative amounts were quantitated using densitometric analysis. Follistatin was distributed in the perinuclear cytoplasm of granulosa and luteal cells but not in theca cells. Dominant follicles contained more (p < 0.05) follistatin than corresponding subordinate follicles. The amount of follistatin was maximal during the mid-growing phase of the dominant follicle and decreased thereafter (p < 0.05). Among the corpora lutea, the maximal amount was detected at mid-diestrus (Day 11 postovulation). Less than half of luteal cells displayed the stain for follistatin; positively stained luteal cells were located in close proximity to blood capillaries. Follistatin was not detectable in the corpus luteum during metestrus (Day 3 postovulation) or proestrus (Day >/= 17 postovulation). In summary, the degree of immunohistochemical expression of follistatin was phase specific for both follicles and corpora lutea. The most intense staining in follicles was associated with the period of functional dominance and in corpora lutea was seen during the phase of maximal development. Significant phase-related differences in follistatin expression provide rationale for the hypothesis that follistatin is involved in the final stages of follicle and luteal gland development in cattle.

Animals↗
PubMedDate not supplied

Mammalian follicular development and atresia: role of apoptosis.

The regulation of follicular development and atresia is a complex process and involves interactions between endocrine factors (gonadotropins) and intraovarian regulators (sex steroids, growth factors and cytokines) in the control of follicular cell fate (i.e. proliferation, differentiation and programmed cell death). Granulosa and theca cells are key players in this fascinating process. As atresia is the fate of most follicles, understanding of how these physiological regulators participate in determining the destiny of the follicle (to degenerate or to ovulate) at cellular and subcellular levels is fundamental. This short review summarizes the role of intraovarian modulators of programmed cell death in the induction of atresia during follicular development.

Animals↗
PubMed1986

Preparation of antiserum to rat cytochrome P-450 cholesterol side chain cleavage, and its use for ultrastructural localization of the immunoreactive enzyme by protein A-gold technique.

Rabbit antiserum to rat cytochrome P-450 cholesterol side chain cleavage (P-450scc) was produced without a previous biochemical purification of the enzyme. Instead, for immunization we used a single protein band of mol wt 53,000, which was isolated from sodium dodecyl sulfate polyacrylamide gel electrophoresis of rat steroidogenic mitochondrial membranes. The resulting antiserum cross-reacted in a protein-blotting test with affinity purified and biologically active bovine adrenocortical P-450scc enzyme. The antiserum to the rat P-450scc also substantially blocked the conversion of cholesterol to pregnenolone in sonicated steroidogenic mitochondria, suggesting a successful cross-reactivity with the native form of the enzyme, despite the fact that the immunizing antigen was sodium dodecyl sulfate-denatured protein. The antiserum was applied for ultrastructural immunocytochemical visualization of the P-450scc in thin sections of adrenal cortex and immature ovary. Immunoreactive enzyme was identified by the protein-A-gold technique which showed that the gold particles concentrated exclusively in the steroidogenic mitochondria of adrenal zona glomerulosa and fasciculata cells. In the immature ovary, the only zone which was heavily stained with colloidal gold was the population of the interstitial cells. Part of the theca cell population contained P-450scc before PMSG treatment. The granulosa cells were devoided of the enzyme in any follicles before the preovulatory stage. The high resolution of the pAg technique allowed to visualize the localization of the P-450scc antigen in the matrix side of the inner mitochondrial membranes. Moreover, a clear coupling could be demonstrated between the morphological and functional maturation of the steroidogenic mitochondrion in the ovary: from a few lamella cristae devoid of P-450scc in the unstimulated granulosa mitochondria, to numerous tubulovesicular inner membranes, heavily loaded with the enzyme, in the mitochondria of the interstitial cells.

Adrenal Cortex↗
PubMed1999

Gonadotropin stimulation of pituitary adenylate cyclase-activating polypeptide (PACAP) messenger ribonucleic acid in the rat ovary and the role of PACAP as a follicle survival factor.

Pituitary adenylate cyclase-activating polypeptide (PACAP), a novel neuropeptide with considerable homology to vasoactive intestinal peptide and GH-releasing hormone, exists in two biologically active forms, PACAP-38 and -27. The presence of PACAP in the ovary has been demonstrated, where it stimulates steroidogenesis and cAMP accumulation in cultured granulosa cells. In the present study, gonadotropin regulation of PACAP gene expression was examined in PMSG/human (h)CG-treated immature rat ovaries and cultured preovulatory follicles. Northern blot analysis of ovaries obtained from PMSG/hCG-treated immature animals revealed the transient induction of PACAP transcripts by hCG, reaching a maximum at 6 h. The major cell types expressing PACAP messenger RNA were granulosa cells of preovulatory follicles and some theca/interstitial cells. In preovulatory follicles cultured in serum-free medium, PACAP transcripts were transiently induced by LH and FSH, reaching a maximum 6-9 h after stimulation in granulosa cells but not in theca cells. Treatment with cycloheximide or alpha-amanitin abolished LH-induced PACAP transcripts, indicating that new protein synthesis and transcription are necessary. Treatment with MDL-12,330A, an inhibitor of adenylate cyclase, inhibited LH-induced PACAP messenger RNA, and forskolin mimicked the LH action, implying the role of adenylate cyclase activation. In contrast, treatment with chelerythrine, an inhibitor of protein kinase C, and 2-O-tetradecanol-phorbol-13-acetate had no effect. We further tested the role of PACAP in follicle apoptosis using apoptotic DNA fragmentation analysis. Treatment with PACAP-38 suppressed follicle apoptosis in a dose-dependent manner. Moreover, the LH suppression of follicle apoptosis was partially blocked by cotreatment with PACAP-38 antagonist, indicating mediation by endogenous PACAP-38. These results suggest that PACAP, transiently induced by the gonadotropin surge, could be a local regulator of a number of events and may act as a follicle survival factor during the periovulatory period.

Adenylyl Cyclases↗
PubMed1997

Ovarian follicular dominance: the role of intraovarian growth factors and novel proteins.

Folliculogenesis is associated with the development of a group of follicles at various stages of maturation from which a species-specific number of follicles are selected for continued growth. These selected follicles, after being exposed to the requisite hormonal environment, ovulate in response to the preovulatory gonadotrophin surge. Follicular dominance is the mechanism by which the selected follicle(s) undergoes rapid development in an environment where growth and development of other follicles, recruited at a similar time, are suppressed. These processes are controlled by the interaction of endocrine signals and locally produced ovarian growth factors. The response of the two major follicular cell types, granulosa and theca cells, to gonadotrophins is regulated by the local production of growth factors. Mechanisms controlling growth factor action occupy a central role in the regulation of folliculogenesis. In this review, we highlight the influence of the extracellular matrix in this process by describing its involvement in regulating the activity of components of the insulin-like growth factor system, transforming growth factor beta superfamily, fibroblast growth factors and the epidermal growth factor/transforming growth factor alpha family. In addition, some recent studies on the role of protein factors produced by the dominant follicle in maintaining dominance and inhibiting the growth of subordinate follicles are described.

Animals↗
PubMed1991

Gynandroblastoma of the ovary. A case report.

An ovarian gynandroblastoma was found in a 59-year-old woman. The tumor consisting of mixed Sertoli-Leydig cells and granulosa-theca cells demonstrated no malignant features. Bisexual cells in gynandroblastoma derived from a common gonadal mesenchyme precursor or indifferent cell. The excision of appendages with tumor or hysterectomy was sufficient.

Female↗
PubMed1988

Oxytocin and ovarian function.

(1) Oxytocin is synthesized in the luteal cells of all species so far studied, including the human. Vasopressin is also synthesized, but at a much lower rate. (2) The oxytocin-neurophysin gene is expressed in granulosa cells and granulosa-derived luteal cells but not in theca cells. Ovulation or spontaneous luteinization initiates the gene expression which peaks in the early luteal phase and ceases around mid-cycle. (3) Luteal oxytocin concentrations rise with considerable delay after the peak of specific mRNA and reach maximal levels around mid-cycle. Oxytocin concentrations fall to low levels in the late luteal phase and in pregnancy. (4) Thecal tissue produces substances such as catecholamines and ascorbic acid that stimulate oxytocin secretion in granulosa cells. The adrenergic innervation of thecal tissue provides a source of catecholamines and may therefore serve a modulatory function in ovarian oxytocin secretion. (5) Oxytocin has little or no direct effect on luteal progesterone production. (6) Oxytocin inhibits LH-stimulated prostacyclin production in luteal cells of cows. Oxytocin may induce the release of PGF-2 alpha or lipo-oxygenase products from the ovary but this has not yet been documented. (7) PGF-2 alpha releases oxytocin from the ovary but does not turn off its synthesis. (8) The concept that ovarian oxytocin participates in the luteolytic process is gaining acceptance. In some species (sheep, goat) ovarian oxytocin acts as a hormone causing PGF-2 alpha release from the uterus. In others it acts in a paracrine or autocrine fashion on ovarian prostanoid production (cow, possibly primates).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Control of steroidogenesis in small and large bovine luteal cells.

Evidence was cited to show that: (1) prostacyclin (PGI2) plays a luteotrophic role in the bovine corpus luteum and that products of the lipoxygenase pathway of arachidonic acid metabolism, especially 5-hydroxyeicosatetraenoic acid play luteolytic roles; (2) oxytocin of luteal cell origin plays a role in development, and possibly in regression, of the bovine corpus luteum; and (3) luteal cells arise from two sources; the characteristic small luteal cells at all stages of the oestrous cycle and pregnancy are of theca cell origin; the large cells are of granulosa cell origin early in the cycle, but a population of theca-derived large cells appears later in the cycle. Results of in vitro studies with total dispersed cells and essentially pure preparations of large and small luteal cells indicate that: (1) the recently described Ca2+-polyphosphoinositol-protein kinase C second messenger system is involved in progesterone synthesis in the bovine corpus luteum; (2) activation of protein kinase C is stimulatory to progesterone synthesis in the small luteal cells; (3) activation of protein kinase C has no effect on progesterone synthesis in the large luteal cells; and (4) protein kinase C exerts its luteotrophic effect in total cell preparations, in part at least, by stimulating the production of prostacyclin. The protein kinase C system may cause down regulation of LH receptors in the large cells.

Animals↗
PubMed2004

Cellular localization and changes in expression of prolactin receptor isoforms in sheep ovary throughout the estrous cycle.

The actions of prolactin (PRL) on target cells depend on the type of prolactin receptor (PRLr) predominantly expressed, particularly whether the long PRLr isoform is expressed. The aims of this study were to determine the cellular localization and the changes in expression of long and short PRLr isoforms in sheep ovary throughout the estrous cycle. Long and short PRLrs were localized mostly in the same ovarian cells. Maximum signal intensity, particularly for long PRLrs, was found in stromal cells surrounding primordial and primary follicles, and, for both PRLrs, in granulosa cells of preantral follicles and in luteal cells. Moderate signal intensity for PRLrs was found in theca cells of preantral to ovulatory follicles, and in granulosa cells of antral follicles up to the gonadotropin-dependent stage. Decreasing immunoreactivity to PRLrs was found in granulosa cells of gonadotropin-dependent to ovulatory follicles. For long PRLrs in particular, no signal was found in mural granulosa cells of gonadotropin-dependent follicles; for both isoforms, no signal was found in most granulosa cells of ovulatory follicles. In primordial to gonadotropin-dependent follicles, cellular localization of PRLr was similar on days 0, 10 and 15 of the cycle. Oocytes consistently showed positive immunostaining for PRLrs. Comparative RT-PCR analysis of long and short PRLr expression showed that the short isoform is evenly expressed throughout the estrous cycle, whereas the expression of the long form increases at the time of estrus and decreases at mid-luteal phase and at the onset of the follicular phase. Expression of long PRLrs was greater than that of short PRLrs on day 0 of cycle; expression of both isoforms was similar on day 10 and on day 15, long PRLrs expression was lower than that of short PRLrs. Our results indicate that in sheep ovary, the maximum responsiveness to PRL might occur during the preovulatory phase of the estrous cycle.

Animals↗
PubMed2000

Localization of oestrogen receptor alpha, oestrogen receptor beta and androgen receptors in the rat reproductive organs.

There is now evidence that oestrogens and androgens can influence male and female reproductive systems. In order to accurately identify the sites of action of oestrogens and androgens, we have proceeded to the histological localization of the two oestrogen receptor (ER) subtypes, ERalpha and ERbeta, and the androgen receptor (AR) in the reproductive tissues of adult rats of both sexes. AR was detected by immunocytochemistry, while ERalpha and ERbeta were localized by both immunocytochemistry and in situ hybridization. In the pituitary gland of animals of both sexes, ERalpha was found in the majority of nuclei of secretory cells in the anterior pituitary. The intermediate and posterior lobes did not show any staining. ERbeta was not found to be expressed in any of the pituitary lobes. Using AR antibodies, nuclear staining was detected in about 50% of secretory cells of the anterior lobe, the intermediate and posterior lobes being completely unstained. In the testis, ERalpha was localized in nuclei of Leydig cells as well as in round spermatocytes and spermatids, while ERbeta could only be detected in Sertoli cell nuclei. AR immunoreactivity was found in nuclei of Sertoli, peritubular myoid and Leydig cells. In the prostate, ERbeta was observed in epithelial cells of tubulo-alveoli, while the stroma was unlabelled. ERalpha was not found to be expressed in any prostate cells. In the prostate, AR was detected in nuclei of epithelial, stromal and endothelial cells. In seminal vesicles, staining of ERalpha was found in nuclei of epithelial and stromal cells. Similar findings were observed using AR antibodies. While ERbeta mRNA could not be detected by in situ hybridization, weak staining for ERbeta was localized in epithelial cells of seminal vesicles. In the ovary, both ERalpha and ERbeta were found to be expressed. ERbeta mRNA was found in granulosa cells of growing follicles, while ERalpha was present in theca cells, interstitial gland cells and germinal epithelium. AR immunoreactivity was detected in granulosa cell nuclei in growing follicles and also in scattered interstitial cells. In the oviduct and uterus, ERalpha was observed in nuclei of epithelial cells as well as of stromal and muscle cells. Similarly, AR immunoreactivity was present in nuclei of epithelial cells, stromal and muscle cells in both the oviduct and uterus. ERbeta was not detected in the oviduct and uterus. The present findings indicate a cell-specific localization of ERalpha, ERbeta and AR in reproductive tissues in rats of both sexes. By establishing the precise sites of action of oestrogens and androgens they contribute to a better understanding of the respective role of these steroids in reproduction function.

Animals↗
PubMed1979

Metabolism of androstenedione by human ovarian tissues in vitro with particular reference to reductase and aromatase activity.

The ability of granulosa and theca cells of the human ovarian follicle at different stages of development, as well as stromal and luteal tissues from human ovaries to metabolize androstenedione (delta 4) to testosterone (T), dihydrotestosterone (DHT), estrone (E1) and estradiol (E2) with or without exposure to additional amounts of folicle-stimulating hormone was investigated by in vitro experiments. The results show that all the aforementioned ovarian tissues metabolized delta 4 to DHT. Indeed, with the exception of estrogen-secreting granulosa cells from large antral follicle (greater than 10 mm diameter) and possibly also luteal tissue from mid-luteal phase ovaries, the various ovarian tissues preferentially metabolized delta 4 to DHT instead of E (E1 + E2). Although thecal tissue is a major source of delta 4 in human ovaries it is concluded that the granulosa cells do not interact with the theca for the synthesis of E as the follicle enlarges from 1 to 10 mm in diameter. Indeed, excessive thecal delta 4 during this growth phase probably inhibits normal follicular development. However, as the follicle enlarges beyond 10 mm in diameter, and as the granulosa cells begin to preferentially metabolize delta 4 to E, the two cell-types of the follicle may increasingly interact to enhance the follicular output of E.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗