Steroidogenesis and apoptosis in the mammalian ovary

Amsterdam, Abraham; Keren-Tal, Iris; Aharoni, Dorit; Dantes, Ada; Land-Bracha, Abigail; Rimon, Ephraim; Sasson, Ravid; Hirsh, Liron

doi:10.1016/j.steroids.2003.09.003

Cited by 81 publications

(38 citation statements)

References 39 publications

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“…Typically, cytoplasmic blebbing and catalytic cleavage events featured during apoptosis commonly lead to loss of function. However, in the cells of the inner layer of the ovarian follicle, the steroidogenic function is preserved through actin migration and a cytoplasmic compartmentalization that segregates and protects steroidogenic machinery from proteosomes activated in the executioner pathways of apoptosis [20][21][22][23]. We found a subtle positive correlation between estradiol and apoptosis, as was reported in a study showing that cultured granulosa cells had an increment in steroidogenesis during programmed cell death [21].…”

Section: Discussionsupporting

confidence: 77%

Effect of GnRH down-regulation on cumulus cell viability and apoptosis as measured by fluorescence-activated cell sorting

Filho¹,

Ribeiro

Rocha

et al. 2008

J Assist Reprod Genet

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Objective To determine whether gonadotropin releasing hormone (GnRH)-agonist or -antagonist induces higher percentages of cumulus cell apoptosis and if the use of either is detrimental to ART outcomes. Patients Women in a private facility under treatment for IVF had their cumulus cells isolated and analyzed by flow cytometry. Viable, apoptotic, and dead cumulus cell rates related to ovarian stimulation by GnRH-agonist orantagonist were measured and compared with fertilization and implantation rates. Results Treatment with GnRH-agonist produced a greater number of follicles than treatment with GnRH-antagonist. No differences in implantation and pregnancy rates were found. While cumulus cell (CC) apoptosis was positively correlated with estradiol on the day of hCG administration, no significant difference in the percentage of apoptotic cells between treatments was detectable. Additionally, implantation rate and the average follicular estradiol production on the day of hCG administration were no different between treatments.Conclusions GnRH-agonist or -antagonist treatment protocols induce similar levels of apoptosis in CCs and are not detrimental to ART outcomes.

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Section: Discussionsupporting

confidence: 77%

Effect of GnRH down-regulation on cumulus cell viability and apoptosis as measured by fluorescence-activated cell sorting

Filho¹,

Ribeiro

Rocha

et al. 2008

J Assist Reprod Genet

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“…However, high levels of intracellular cAMP could enhance steroidogenesis and at the same time induce apoptosis in granulosa cells, which may be related to recruitment of primordial follicles, initiation of folliculogenesis, and preparation for a proper response to FSH elevation at the beginning of the subsequent ovarian cycle. It is known that degeneration of the old corpora lutea in each estrous/menstrual cycle by programmed cell death is essential for maintenance of normal cyclicity of ovarian steroidogenesis [40,46]. Based on comparison with the gonadotropin-primed i m m a t u r e r a t m o d e l s 2 4 h a f t e r h C G administration, the different patterns of temporal changes in cAMP concentrations on the day of estrus in the adult rats further imply that there are differences between immature and adult rats in regard to the complex mechanisms in regulation of the cAMP system; these differences may be due, in part, to the remnants of previous corpora lutea.…”

Section: Discussionmentioning

confidence: 99%

Changes of Cyclic AMP Levels and Phosphodiesterase Activities in the Rat Ovary

Wang

Wei

Jiang

et al. 2007

Journal of Reproduction and Development

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Abstract. Cyclic AMP (cAMP) is a second messenger that plays a critical role in follicular recruitment, development and luteinization in the mammalian ovary. The cellular level of cAMP is largely dependent on the activity of phosphodiesterase (PDE), which degrades cAMP into 5'-AMP. The present study was conducted to investigate the level of cAMP and the activity of cAMP-PDE in postnatal rats; immature rats during gonadotropin-primed follicular development, ovulation and luteinization; adult rats during normal estrous cycling; and aged rats that spontaneously developed persistent estrous (PE) by radioimmunoassay (RIA). All four rat models were confirmed by histological examination of one ovary and assayed using the other ovary by RIA. In the postnatal rats, the ovarian cAMP level was high on day 10 after birth, while ovarian cAMP-PDE activity was highest at 21 days of age. In the immature female rats, both the ovarian cAMP level and cAMP-PDE activity increased remarkably after treatment with equine chorionic gonadotropin (eCG), increased continuously 24 h after injection of human chorionic gonadotropin (hCG) for induction of ovulation and luteinization, and then declined significantly. In the adult rats during the normal estrous cycle, the ovarian cAMP levels were low on the day of estrus, and there were no significant changes in ovarian cAMP-PDE activity throughout the estrous cycle. In the PE rats, the ovarian cAMP levels were similar to those of the adult rats on the day of estrus but were lower than those on the other days of the estrous cycle; ovarian cAMP-PDE activity was lower than that in the adult rats on any day of the estrous cycle. Together, these findings indicate that the ovarian cAMP level and cAMP-PDE activity were regulated in a stage-dependent manner during ovarian follicular development, atresia and luteinization and providing evidences that cAMP and cAMP-specific PDEs are involved in these physiological processes.

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“…MAPKs, PI3K/Akt, CDKs, TKs, ALK, and AK probably inhibit this process (Sirotkin andMakarevich, 1999, 2002;Makarevich et al, 2002Makarevich et al, , 2004aWang and Tsang, 2007;Macarulla et al, 2008), and PKG stimulates it (Sirotkin et al, 2000a). cAMP/PKA can either up-regulate (Spaczynski et al, 2005;Amsterdam et al, 2003)-, dow-regulate (Viegas et al, 2008)-or not affect (Sirotkin andMakarevich, 1999, 2002;Sirotkin, 2005; Fig. 4) ovarian cell apoptosis.…”

Section: Protein Kinases Control Ovarian Cell Apoptosismentioning

confidence: 99%

Protein kinases and ovarian functions

Sirotkin

Makarevich

Grosmann³

2010

Journal Cellular Physiology

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The present focus survey represents a short review of current knowledge concerning involvement of protein kinases in control of basic ovarian functions. Ovarian cells produce a number of protein kinases, whose expression depends on type of cells, their state and action of hormones and other protein kinases. A number of protein kinases are involved in control of ovarian cell proliferation, apoptosis, oocyte maturation, hormone release, reception and response to hormones, as well as in mediating action of hormones on these ovarian functions. Complexity of interrelationships between different protein kinase-dependent signaling pathways occurs. Protein kinases and their regulators could be used for characterization, prediction and control of ovarian folliculogenesis and atresia, Corpus luteum functions, oocyte maturation, fertility, release of hormones, response of ovarian structures to hormonal regulators, as well as for treatment of some reproductive disorders. The present data demonstrate importance of protein kinases in control of basic ovarian function and potential usage of protein kinases for characterization, prediction and control of these functions.

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Steroidogenesis and apoptosis in the mammalian ovary

Cited by 81 publications

References 39 publications

Effect of GnRH down-regulation on cumulus cell viability and apoptosis as measured by fluorescence-activated cell sorting

Effect of GnRH down-regulation on cumulus cell viability and apoptosis as measured by fluorescence-activated cell sorting

Changes of Cyclic AMP Levels and Phosphodiesterase Activities in the Rat Ovary

Protein kinases and ovarian functions

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