The Experts below are selected from a list of 288 Experts worldwide ranked by ideXlab platform
Jo Anne S. Richards - One of the best experts on this subject based on the ideXlab platform.
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ccaat enhancer binding proteins c ebp α and β are essential for ovulation Luteinization and the expression of key target genes
Molecular Endocrinology, 2011Co-Authors: Peter F Johnson, Jo Anne S. RichardsAbstract:The transcription factors C/EBPα/β are targets of ERK1/2 and control genes associated with Luteinization and the formation of extensive vascular networks that sustain luteal cells.
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β catenin ctnnb1 promotes preovulatory follicular development but represses lh mediated ovulation and Luteinization
Molecular Endocrinology, 2010Co-Authors: Annalouise Oconnor, Manami Shitanaka, Masayuki Shimada, Jo Anne S. RichardsAbstract:Wingless-type mouse mammary tumor virus integration site family (WNT)/β-catenin (CTNNB1) pathway components are expressed in ovarian granulosa cells, direct female gonad development, and are regulated by the pituitary gonadotropins. However, the in vivo functions of CTNNB1 during preovulatory follicular development, ovulation, and Luteinization remain unclear. Using a mouse model Ctnnb1(Ex3)fl/fl;Cyp19-Cre (Ctnnb1(Ex3)gc−/−), expressing dominant stable CTNNB1 in granulosa cells of small antral and preovulatory follicles, we show that CTNNB1 facilitates FSH-induced follicular growth and decreases the follicle atresia (granulosa cell apoptosis). At the molecular level, WNT signaling and FSH synergistically promote the expression of genes required for cell proliferation and estrogen biosynthesis, but decrease FOXO1, which negatively regulates proliferation and steroidogenesis. Conversely, dominant stable CTNNB1 represses LH-induced oocyte maturation, ovulation, Luteinization, and progesterone biosynthesis. S...
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novel signaling pathways that control ovarian follicular development ovulation and Luteinization
Recent Progress in Hormone Research, 2002Co-Authors: Jo Anne S. Richards, Darryl L Russell, Scott A Ochsner, Minnie Hsieh, Kari M H Doyle, Allison E Falender, Yuet Lo, Susan SharmaAbstract:: The interactions of peptide and steroid hormone signaling cascades in the ovary are critical for follicular growth, ovulation, and Luteinization. Although the pituitary gonadotropins follicle-stimulating hormone (FSH) and luteinizing hormone (LH) play key regulatory roles, their actions are also dependent on other peptide signaling pathways, including those stimulated by insulin-like growth factor-1 (IGF-1), transforming growth factor-beta (TGF-beta) family members (e.g., inhibin, activin, growth differentiation factor-9, bone morphogenic proteins), fibroblast growth factor, and Wnts (via Frizzled receptors). Each of these factors is expressed and acts in a cell-specific manner at defined stages of follicular growth. IGF-1, estrogen, and FSH comprise one major regulatory system. The Wnt/Frizzled pathways define other aspects relating to ovarian embryogenesis and possibly ovulation and Luteinization. Likewise, the steroid receptors as well as orphan nuclear receptors and their ligands impact ovarian cell function. The importance of these multiple signaling cascades has been documented by targeted deletion of specific genes. For example, mice null for the LH-induced genes progesterone receptor (PR) and cyclo-oxygenase-2 (COX-2) fail to ovulate. Whereas PR appears to regulate the induction of novel proteases, COX-2 appears to regulate cumulus expansion. This review summarizes some new aspects of peptide and steroid hormone signaling in the rodent ovary.
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Molecular mechanisms of ovulation and Luteinization
Molecular and Cellular Endocrinology, 1998Co-Authors: Jo Anne S. Richards, Maya Dajee, Darryl L Russell, Rebecca L. Robker, Tamara N. AllistonAbstract:Ovulation is a complex process initiated by the mid-cycle surge of luteinizing hormone (LH). Once initiated, a cascade of events occurs that culminates in the release of a fertilizable oocyte. The complex series of events involves specific ovarian cell types, diverse signaling pathways and temporally controlled expression of specific genes. This review will focus on several genes shown to control the ovulation process.
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luteinizing hormone induces prostaglandin endoperoxide synthase 2 and Luteinization in vitro by a kinase and c kinase pathways
Endocrinology, 1995Co-Authors: Jacqueline K Morris, Jo Anne S. RichardsAbstract:The LH surge induces ovulation [prostaglandin synthase-2 (PGS-2)] and Luteinization (progesterone synthesis) of preovulatory follicles by cAMP-dependent mechanisms. Peptides, such as GnRH and angiotensin-II, that activate other cellular signaling pathways have been shown to mimic some of the effects of LH. Therefore, the relative functional importance of different cellular signaling pathways in mediating the induction of PGS-2 and Luteinization was analyzed using the agonists (LH, GnRH, and angiotensin-II) and selective inhibitors of A-kinase (H-89), C-kinase (calphostin-C), and calmodulin kinase-II (KN93). LH or GnRH, but not angiotensin-II, markedly induced PGS-2 protein in preovulatory follicles. H-89 and calphostin-C, but not KN93 inhibited LH induction of PGS-2, whereas calphostin-C selectively blocked induction by GnRH. In contrast, the A- and C-kinase inhibitors prevented both LH and GnRH induction of granulosa cell Luteinization. Taken together, these results provide biological evidence that the r...
P Devroey - One of the best experts on this subject based on the ideXlab platform.
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progesterone rise on the day of human chorionic gonadotropin administration impairs pregnancy outcome in day 3 single embryo transfer while has no effect on day 5 single blastocyst transfer
Fertility and Sterility, 2009Co-Authors: E G Papanikolaou, Andre Van Steirteghem, Efstratios M Kolibianakis, Cristina Pozzobon, Parikshit Tank, H Tournaye, C Bourgain, P DevroeyAbstract:Four hundred eighty-two patients undergoing single ET with GnRH-antagonist/recFSH protocol were analyzed. The incidence of premature Luteinization (P above 1.5 ng/mL on the day of hCG administration) was 18.2%. Even modest rises of P in the follicular phase have detrimental effect on the implantation potential of a good-quality cleavage stage embryo. On the contrary, premature Luteinization in the blastocyst subgroup had no effect on the pregnancy outcome
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premature Luteinization in in vitro fertilization cycles using gonadotropin releasing hormone agonist gnrh a and recombinant follicle stimulating hormone fsh and gnrh a and urinary fsh
Fertility and Sterility, 1996Co-Authors: F Ubaldi, Marguerite Camus, Johan Smitz, Herjan Coelingh J T Bennink, Andre Van Steirteghem, P DevroeyAbstract:Abstract Objective: To determine if premature Luteinization can occur in GnRH agonist (GnRH-a) and FSH (recombinant FSH and human urinary FSH) IVF cycles and whether premature Luteinization affects IVF and clinical outcome. Design: Retrospective evaluation of 171 IVF-ET cycles. The cycles were divided into two groups according to the P level on the day of hCG: group I (serum P ≤ 0.9 ng/mL [conversion factor to SI unit, 3.180]) and group II (serum P ≥ 1.1 ng/mL). Main Outcome Measure(s): Comparison of cycles characteristics and of cumulative exposure of follicular serum E 2 , FSH, LH, and P as well as of IVF and clinical outcome were made between the study groups. Result(s): Twenty-three of 171 cycles (13.4%) demonstrated premature Luteinization. The age of the patients, the E 2 , and LH exposure were similar between the groups. The number of the ampules of gonadotropins (recombinant FSH and urinary FSH) used and the area under FSH and P curve were higher in cycles with premature Luteinization. The area under the FSH curve correlated with the area under the P curve. Similar IVF and clinical outcomes were observed in cycles with and without premature Luteinization. Conclusion(s): The greater FSH exposure and its correlation with the P exposure suggest that one of the possible factors inducing premature Luteinization is the increased FSH-induced LH receptivity in granulosa cells. No adverse effects of premature Luteinization on the IVF and clinical outcome were observed.
Bruce D Murphy - One of the best experts on this subject based on the ideXlab platform.
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CHAPTER 11 – Luteinization
The Ovary, 2020Co-Authors: Bruce D MurphyAbstract:A morphological and biochemical remodeling process known as Luteinization ensues following rupture of the preovulatory ovarian follicle, resulting in the formation of a transient but essential ovarian organ called the corpus luteum (CL). In most species studied, the two endocrine cells of the follicle, the theca cells and the granulosa cells, contribute to the CL. The process of Luteinization includes modification of expression of steroidogenic enzymes and the steroidogenic acute regulatory protein to bring about large-scale synthesis of progesterone by the CL. There are concomitant changes in expression of proteins that provide cholesterol, the parent molecule for steroidogenesis to the luteal cells, including the low- and high-density lipoprotein receptors and the intracellular cholesterol delivery protein, known as the Niemann-Pick C-l protein (NPC-1). Luteinization is a process of terminal differentiation of the component steroidogenic cells and thus consists of the exit from the cell cycle, occurring first in the granulosa cell component and then more gradually in the theca cells of the CL. Removal of the oocyte from a follicle provokes Luteinization, which suggests inhibitory control. Nonetheless, the usual in vivo stimulus for Luteinization is the preovulatory luteinizing hormone (LH) surge, and LH can induce Luteinization of follicles that contain an oocyte, which indicates multiple levels of control. The most important intracellular pathway regulating formation of the CL is the cyclic adenosine monophosphate (cAMP)-protein kinase A cascade. Recent investigation has shed light on the molecular mechanisms of Luteinization. Transactivation by several transcription factors induces the expression of the genes that mark the Luteinization process. Luteinization is associated with a covalent modification of the deoxyribonucleic acid (DNA) packaging proteins, histone H3 and H4. In conclusion, Luteinization is a coordinated program of gene expression that brings about an extensive change in two cell types of the ovarian follicle, resulting in a focus on the synthesis of progesterone.
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lipoprotein receptor expression during Luteinization of the ovarian follicle
American Journal of Physiology-endocrinology and Metabolism, 2007Co-Authors: Leonor Mirandajimenez, Bruce D MurphyAbstract:Ovarian follicles luteinize after ovulation, requiring structural and molecular remodeling along with exponential increases in steroidogenesis. Cholesterol substrates for luteal steroidogenesis are imported via scavenger receptor-BI (SR-BI) and the low-density lipoprotein (LDL) receptor from circulating high-density lipoproteins and LDL. SR-BI mRNA is expressed in pig ovaries at all stages of folliculogenesis and in the corpus luteum (CL). An 82-kDa form of SR-BI predominates throughout, is weakly present in granulosa cells, and is robustly expressed in the CL, along with the less abundant 57-kDa form. Digestion of N-linked carbohydrates substantially reduced the SR-BI mass in luteal cells, indicating that differences between forms is attributable to glycosylation. Immunohistochemistry revealed SR-BI to be concentrated in the cytoplasm of follicular granulosa cells, although found mostly at the periphery of luteal cells. To examine receptor dynamics during gonadotropin-induced Luteinization, pigs were treated with an ovulatory stimulus, and ovaries were collected at intervals to ovulation. SR-BI in granulosa cell cytoplasm increased through the periovulatory period, with migration to the cell periphery as the CL matured. In vitro culture of follicles with human chorionic gonadotropin induced time-dependent upregulation of 82-kDa SR-BI in granulosa cells. SR-BI and LDL receptor were reciprocally expressed, with the latter highest in follicular granulosa cells, declining precipitously with CL formation. We conclude that Luteinization causes upregulation of SR-BI expression, its posttranslational maturation by glycosylation, and insertion into luteal cell membranes. Expression of the LDL receptor is extinguished during Luteinization, indicating dynamic regulation of cholesterol importation to maintain elevated steroid output by the CL.
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models of Luteinization
Biology of Reproduction, 2000Co-Authors: Bruce D MurphyAbstract:Luteinization is essential to the success of early gestation. It is the process by which elements of the ovarian follicle, usually including both theca interna and granulosa cells, are provoked by the ovulatory stimulus to develop into the corpus luteum. Although there are significant species differences in Luteinization, some elements pervade, including the morphological and functional differentiation to produce and secrete progesterone. There is evidence that Luteinization results in granulosa cell exit from the cell cycle. The mechanisms that appear to control Luteinization include intracellular signalling pathways, cell adhesion factors, intracellular cholesterol and oxysterols, and perhaps progesterone itself as a paracrine or intracrine regulator. Cell models of Luteinization, along with some of the conflicting observations on the Luteinization process, are discussed in this review.
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growth factor modulation of steroidogenic acute regulatory protein and Luteinization in the pig ovary
Biology of Reproduction, 1999Co-Authors: Nazario Pescador, Douglas M Stocco, Bruce D MurphyAbstract:In vivo and in vitro Luteinization were investigated in the porcine ovary, with emphasis on expression of steroidogenic acute regulatory protein (StAR). StAR mRNA and protein as well as cytochrome P450 side-chain cleavage mRNA (P450 scc ) increased during the luteal phase in the corpus luteum (CL) and were absent in regressed CL. Cytochrome P450 aromatase mRNA (P450 arom ) was not detectable at any time in CL. In vitro Luteinization of granulosa cells occurred over 96 h in culture, during which P450 arom mRNA was present at 1 h after cell isolation but not detectable at 6 h; and P450 scc and StAR mRNAs were first detectable at 6 h and 48 h, respectively. Incubation of cultures with insulin-like growth factor I (IGF-I, 10 ng/ml), dibutyryl cAMP (cAMP, 300 μM), or their combination, induced measurable StAR mRNA at 24 h (p < 0.05), increased progesterone accumulation at 48 h, and elevated both StAR and P450 scc expression through 96 h. Incubation of luteinized granulosa cells with epidermal growth factor (EGF, 10 nM) changed their phenotype from epithelioid to fibroblastic, eliminated steady-state StAR expression, and interfered with cAMP induction of StAR mRNA and progesterone accumulation. EGF had little apparent effect on P450 scc mRNA abundance. It is concluded that StAR expression characterizes Luteinization, and early Luteinization is induced by cAMP and IGF-I in vitro. Further, EGF induces a morphological and functional phenotype that appears similar to an earlier stage of granulosa cell function.
Jacqueline K Morris - One of the best experts on this subject based on the ideXlab platform.
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luteinizing hormone induces prostaglandin endoperoxide synthase 2 and Luteinization in vitro by a kinase and c kinase pathways
Endocrinology, 1995Co-Authors: Jacqueline K Morris, Jo Anne S. RichardsAbstract:The LH surge induces ovulation [prostaglandin synthase-2 (PGS-2)] and Luteinization (progesterone synthesis) of preovulatory follicles by cAMP-dependent mechanisms. Peptides, such as GnRH and angiotensin-II, that activate other cellular signaling pathways have been shown to mimic some of the effects of LH. Therefore, the relative functional importance of different cellular signaling pathways in mediating the induction of PGS-2 and Luteinization was analyzed using the agonists (LH, GnRH, and angiotensin-II) and selective inhibitors of A-kinase (H-89), C-kinase (calphostin-C), and calmodulin kinase-II (KN93). LH or GnRH, but not angiotensin-II, markedly induced PGS-2 protein in preovulatory follicles. H-89 and calphostin-C, but not KN93 inhibited LH induction of PGS-2, whereas calphostin-C selectively blocked induction by GnRH. In contrast, the A- and C-kinase inhibitors prevented both LH and GnRH induction of granulosa cell Luteinization. Taken together, these results provide biological evidence that the r...
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Molecular Regulation of Genes Involved in Ovulation and Luteinization
Ovarian Cell Interactions, 1993Co-Authors: Jo Anne S. Richards, Jacqueline K Morris, Jean Sirois, Usha Natraj, Susan L. Fitzpatrick, Jeffrey W. ClemensAbstract:Two principal physiological events occur within preovulatory follicles as a consequence of the LH/FSH surge: ovulation and Luteinization. The ovulation process culminates in the extrusion of the oocyte-cumulus complex and is dependent on a specific sequence of biochemical events. These biochemical changes include the rapid but transient increase in a novel, distinct isoform of prostaglandin endoperoxide synthase (PGS-2) (1–8), tissue plasminogen activator (tPA) (9, 10), and progesterone receptor (PR) (11–13). In contrast, Luteinization is a process by which follicular granulosa and theca cells become nonmitotic and establish a specific, stable luteal cell phenotype. The biochemical changes that occur in response to the LH surge and are associated with Luteinization include the marked and sustained induction of cholesterol side-chain cleavage cytochrome P450 (P450scc), as well as the dramatic and rapid decreases in mRNA for the LH receptor (LH-R), the regulatory subunit β of type II cyclic AMP-dependent protein kinase (RIIβ), aromatase, and 17α-hydroxylase (P45017α) (Fig. 10.1) (14). Once Luteinization has occurred, genes regulated by FSH/LH/cAMP in the follicle are no longer regulated by these agonists in the corpus luteum. This apparent transition from cAMP-dependent regulation to cAMP-independent regulation of these genes has prompted us to ask why surge (as opposed to basal) concentrations of LH are required to initiate these two diverse processes, what might be unique about the genes induced by the LH surge, and what intracellular signaling pathways might be involved.
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hormone induction of Luteinization and prostaglandin endoperoxide synthase 2 involves multiple cellular signaling pathways
Endocrinology, 1993Co-Authors: Jacqueline K Morris, Jo Anne S. RichardsAbstract:To determine the cellular signaling pathways involved in granulosa cell Luteinization, known activators of protein kinase-A (LH and FSH) and protein kinase-C [GnRH and phorbol 12-myristate 13-acetate (PMA)] as well as inhibitors of tyrosine kinases (AG18 and genistein) were tested in an in vitro system using specific markers of Luteinization (cell hypertrophy, side-chain cleavage cytochrome P450, and progesterone) and ovulation [prostaglandin endoperoxide synthase-2 (PGS-2)]. When preovulatory follicles were incubated in the presence of an ovulatory (500 ng/ml) dose of LH or high GnRH (1 microM), the granulosa cells harvested from these follicles assumed and maintained a stable luteal cell phenotype in vitro. Granulosa cells harvested from follicles incubated in subovulatory doses of LH (5 and 50 ng/ml), lower doses of GnRH (5, 50, and 500 nM), or PMA alone were unable to form a stable luteal cell phenotype. When PMA was combined with subovulatory doses of LH, granulosa cells luteinized, and PGS-2 protein...
S Mashiach - One of the best experts on this subject based on the ideXlab platform.
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management of women with polycystic ovary syndrome who experienced premature Luteinization during clomiphene citrate treatment
Fertility and Sterility, 2000Co-Authors: Arie L Lidor, Mordechai Goldenberg, Shlomo B Cohen, Daniel S Seidman, S MashiachAbstract:Abstract Objective: To determine the preferred treatment modality in patients with PCOS who experienced premature Luteinization during CC treatment. Design: Prospective randomized study. Setting: Tertiary medical center. Patients: Twenty-two infertile women with PCOS demonstrating premature Luteinization during at least two consecutive CC cycles. Interventions: Randomized induction of ovulation either with FSH alone or with GnRH agonist combined with FSH for a single treatment cycle. Main Outcome Measures: Premature Luteinization was defined as serum progesterone >1.5 ng/mL before hCG administration. Results: Premature Luteinization occurred in eight of the 10 patients (80%) in group A and in two of the 12 patients in group B (16.6%). This result corresponds to the higher mean (±SD) progesterone level present in group A patients as compared to those in group B (2.0 ± 1.2 ng/mL vs. 1.2 ± 0.6 ng/mL, P =0.03). No pregnancies were achieved in group A, whereas the pregnancy rate per cycle observed in group B was 33.3% (4/12). On the day of hCG administration, the maximum mean (±SD) estradiol level was significantly lower ( P Conclusions: Pituitary desensitization with GnRH analog in combination with FSH is superior to FSH-only treatment in PCOS patients who demonstrate premature Luteinization during CC treatment.
