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1 - Folliculogenesis: From Preantral Follicles to Corpus Luteum Regression

from PART I - PHYSIOLOGY OF REPRODUCTION

Published online by Cambridge University Press:  04 August 2010

Botros R. M. B. Rizk
Affiliation:
University of South Alabama
Juan A. Garcia-Velasco
Affiliation:
Rey Juan Carlos University School of Medicine,
Hassan N. Sallam
Affiliation:
University of Alexandria School of Medicine
Antonis Makrigiannakis
Affiliation:
University of Crete
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Summary

INTRODUCTION

The most common function of the female gonad is to produce gametes, the oocytes, and sex hormones, such as estrogens and progesterone, which control the development of the female secondary sexual characteristics and support pregnancy. These two functions are exerted cyclically between puberty and the menopause, and they are regulated by diverse endocrine and paracrine factors acting on many cell types situated in the ovary. Ovarian functions result from the evolution of a morphological unit, the ovarian follicle, which consists of a central oocyte surrounded by granulosa cells and other layers of somatic theca cells (1). The maturation of the follicle proceeds through primordial, primary, and secondary stages of development and is controlled by various factors produced in the ovary. The main physiological stimulants for differentiation and luteinization of granulosa cells, which are a main cellular component of the follicle, are the gonadotropin hormones, follicle-stimulating hormone (FSH), and luteinizing hormone (LH). Throughout the reproductive life span of the female, only limited number of follicles will reach the stage of Graafian follicle and will ovulate, whereas the vast majority is gradually eliminated through a process called atresia. In every menstrual cycle, only one follicle, named the dominant follicle, is destined to complete maturation and ovulate, and thus, the formation of the multiple embryos during pregnancy is prevented.

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Publisher: Cambridge University Press
Print publication year: 2008

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References

McGee, EA, Hsueh, AJ. 2000. Initial and cyclic recruitment of ovarian follicles. Endocr Rev 21:200–14.Google ScholarPubMed
Fair, T. 2003. Follicular oocyte growth and acquisition of developmental competence. Anim Reprod Sci 15:203–16.CrossRefGoogle Scholar
Markström, E, Svensson, EC, Shao, R, et al. 2002. Survival factors regulating ovarian apoptosis—dependence on follicle differentiation. Reproduction 123:23–30.CrossRefGoogle ScholarPubMed
Zeleznik, JA. 2004. The physiology of follicle selection. Reprod Biol Endocrinol 2:31–7.CrossRefGoogle ScholarPubMed
Rizk, B (Ed.). 2008. Ultrasonography in reproductive medicine and infertilityCambridge, UK: Cambridge University Press, (in press).Google Scholar
Touraine, P, Beau, I, Gougeon, A, et al. 1999. New natural inactivating mutations of the follicle-stimulating hormone receptor: correlations between receptor function and phenotype. Mol Endocrinol 13:1844–54.CrossRefGoogle ScholarPubMed
Visser, JA, Themmen, AP. 2005. Anti-Mullerian hormone and folliculogenesis. Mol Cell Endocrinol 234:81–6.CrossRefGoogle ScholarPubMed
Roy, SK, Treacy, BJ. 1993. Isolation and long-term culture of human preantral follicles. Fertil Steril 59:783–90.CrossRefGoogle ScholarPubMed
Barboni, B, Turriani, M, Galeati, G, et al. 2000. Vascular endothelial growth factor production in growing pig antral follicles. Biol Reprod 63:858–64.CrossRefGoogle ScholarPubMed
Kaczmarek, MM, Schams, D, Ziecik, JA. 2005. Role of the vascular endothelial growth factor in ovarian physiology—an overview. Reprod Biol 5:111–36.Google Scholar
Waltenberger, J, Claesson-Welsh, L, Siegbahm, A, et al. 1994. Different signal transduction properties of KDR and Flt-1, two receptors for vascular endothelial growth factor. J Biol Chem 269:26988–95.Google ScholarPubMed
Filicori, M, Cognigni, EG. 2001. Roles and novel regimens of luteinizing hormone and follicle stimulating hormone in ovulation induction. J Clin Endocrinol Metab 86:1437–41.Google ScholarPubMed
Rizk, B. 2006. Genetics of ovarian hyperstimulation syndrome. In Rizk, B Ed.), Ovarian Hyperstimulation Syndrome. Cambridge, New York: Cambridge University Press, Chapter 4, pp. 79–91.Google Scholar
Filicori, M, Cognigni, EG, Tabarelli, C, et al. 2002. Stimulation and growth of antral ovarian follicles by selective LH activity administration in women. J Clin Endocrinol Metab 87:1156–61.CrossRefGoogle ScholarPubMed
Mohri, H. 1996. Fibronectin and integrins interactions. J Invest Med 44:429–41.Google ScholarPubMed
Senger, DR, Claffey, KP, Benes, JE, et al. 1997. Angiogenesis promoted by vascular endothelial growth factor: regulation through α1β1 and α2β1 integrins. Proc Natl Acad Sci USA 94:13612–17.CrossRefGoogle ScholarPubMed
Vaskivuo, TE, Ottander, U, Oduwole, O et al. 2002. Role of apoptosis, apoptosis-related fectors and 17beta-hydroxysteroid dehydrogenases in human corpus luteum regression. Mol Cell Endocrinol 30:191–200.CrossRefGoogle Scholar
Vaskivuo, TE, Tapanainen, JS. 2003. Apoptosis in the human ovary. Reprod BioMed Online 6(1):24–35.CrossRefGoogle ScholarPubMed
Rodger, FE, Fraser, HM, Krajewski, S, et al. 1998. Production of the proto-oncogene Bax does not vary with changing in luteal function in women. Mol Hum Reprod 4:27–32.CrossRefGoogle Scholar
Sugino, N, Suzuki, T, Kashida, S, et al. 2000. Expression of Bcl-2 and Bax in the human corpus luteum during the menstrual cycle and in early pregnancy: regulation by human chorionic gonadotropin. J Clin Endocrinol Metabol 85:4379–86.Google ScholarPubMed
Rolaki, A, Drakakis, P, Millingos, S, et al. 2005. Novel trends in follicular development, atresia and corpus luteum regression: a role for apoptosis. Reprod Biomed Online 11:93–103.CrossRefGoogle ScholarPubMed
Amsterdam, A, Gold, RS, Hosokawa, K, et al. 1999. Crosstalk among multiple signaling pathways controlling ovarian cell death. Trends Endocrinol Metabol 10:255–62.CrossRefGoogle ScholarPubMed
Oosterhuis, GJE, Michgelsen, HW, Lambalk, CB, et al. 1998. Apoptotic cell death in human granulosa-lutein cells: a possible indicator of in vitro fertilization outcome. Fertil Steril 4:747–9.CrossRefGoogle Scholar
Idil, M, Cepni, I, Demirsoy, G, et al. 2004. Does granulosa cell apoptosis have a role in the etiology of unexplained infertility?Eur J Obstet Gynecol Reprod Biol 112:182–4.CrossRefGoogle ScholarPubMed
Kaelin, WG Jr. 1999. Cancer. Many vessels, faulty gene. Nature 399:203–4.CrossRefGoogle ScholarPubMed
Davies, R, Moore, A, Schedl, A, et al. 1999. Multiple roles for the Wilms' tumor suppressor, WT1. Cancer Res 59:1747–50.Google ScholarPubMed
Tilly, JL, Tilly, KI. 1995. Inhibitors of oxidative stress mimic the ability follicle-stimulating hormone to suppress apoptosis in cultured rat ovarian follicles. Endocrinology 136:242–52.CrossRefGoogle ScholarPubMed
Kim, JM, Yoon, YD, Tsang, BK. 1999. Involvement of the Fas/Fas ligand system in p53-mediated granulosa cell apoptosis during follicular development and atresia. Endocrinology 140: 2307–17.CrossRefGoogle ScholarPubMed
Kugu, K, Ratts, VS, Piquette, GN, et al. 1998. Analysis of apoptosis and expression of bcl-2 gene family members in the human and baboon ovary. Cell Death Differen 5:67–76.CrossRefGoogle ScholarPubMed
Hosokawa, K, Aharoni, D, Dantes, A, et al. 1998. Modulation of Mdm2 expression and p53-induced apoptosis in immortalized human ovarian granulosa cells. Endocrinology 139:4688–700.CrossRefGoogle ScholarPubMed
Makrigiannakis, A, Amin, K, Coukos, G, et al. 2000. Regulated expression and potential roles of p53 and Wilms' tumor suppressor gene (WT1 during follicular development in the human ovary). J Clin Endocrinol Metab 85:449–59.Google Scholar
Quirk, MS, Cowan, GR, et al. 2003. Ovarian follicular growth and atresia: the relationship between cell proliferation and survival. J Anim Sci 82:40–52.CrossRefGoogle Scholar
Sasson, R, Winder, N, Kees, S, Amsterdam, A. 2002. Induction of apoptosis in granulosa cells by TNFα and its attenuation by glucocorticoids involve modulation of Bcl-2. Biochem Biophys Res Com 294:51–9.CrossRefGoogle ScholarPubMed
Knudson, CM, Tung, KSK, Tourtellotte, WG, et al. 1995. Bax-deficient mice with lymphoid hyperplasia and male germ cell death. Science 270:96–99.CrossRefGoogle ScholarPubMed
Drummond, EA. 2006. The role of steroids in follicular growth. Reprod Biol Endocrinol 4:16–26.CrossRefGoogle ScholarPubMed
Robker, RL, Russell, DL, Espey, LL, et al. 2000. Progesterone-regulated genes in the ovulation process: ADAMTS-1 and cathepsin L proteases. Proc Natl Acad Sci USA) 97:4689–94.CrossRefGoogle ScholarPubMed
Polt, SP, Leung, K, et al. 2002. Roles of cyclic GMP in modulating ovarian functions. Reprod Biomed Online 6:15–23.Google Scholar
Natraj, U, Richards, JS. 1993. Hormonal regulation, localisation and functional activity of the progesterone receptor in granulosa cells of rat preovulatory follicles. Endocrinology 133:761–9.CrossRefGoogle Scholar
Zalanyi, S. 2001. Progesterone and ovulation. Eur J Obstet Gynecol Reprod Biol 98:152–9.CrossRefGoogle ScholarPubMed
Makrigiannakis, A, Coukos, G, Christofidou-Solomidou, M, et al. 2000. Progesterone is an autocrine/paracrine regulator of human granulosa cell survival in vitro. Ann N Y Acad Sci 900:16–25.CrossRefGoogle ScholarPubMed
Steckler, T, Wang, J, Bartol, FF, et al. 2005. Fetal programming: prenatal testosterone treatment causes intrauterine growth retardation, reduces ovarian reserve and increases ovarian follicular recruitment. Endocrinology3185–93.CrossRefGoogle ScholarPubMed
Vendola, KA, Zhou, J, Adesanya, OO, et al. 1998. Androgens stimulate early stages of follicular growth in the primate ovary. J Clin Investig 101:2622–9.CrossRefGoogle ScholarPubMed
Hillier, SG, Zwart, FA. 1981. Evidence that granulosa cell aromatase induction/activation by follicle-stimulating hormone is an androgen receptor-regulated process in-vitro. Endocrinology 109:1303–5.CrossRefGoogle ScholarPubMed
Abbott, DH, Dumesic, DA, Franks, S. 2002. Developmental origin of polycystic ovary syndrome—a hypothesis. J Endocrinol 174: 1–5.CrossRefGoogle ScholarPubMed
Leo, V, Lanzetta, D, D'Antona, D, et al. 1998. Hormonal effects of flutamide in young women with polycystic ovary syndrome. J Clin Endocrinol Metab 83:99–102.CrossRefGoogle ScholarPubMed
Hegele-Hartung, C, Seibel, P, Peters, O, et al. 2004. Impact of isotype-selective oestrogen receptor agonists on ovarian function. Proc Natl Acad Sci USA) 101:5129–34.CrossRefGoogle ScholarPubMed
Makrigiannakis, A, Coukos, G, Christofidou-Solomidou, M, et al. 1999 N-cadherin mediated human granulosa cell adhesion prevents apoptosis: a role in follicular atresia and luteolysis?Am J Pathol 154:1391–406.CrossRefGoogle ScholarPubMed
Knudsen, KA, Soler, AP, Johnson, KR et al. 1995. Interaction of a-actinin with the cadherin cell-cell adhesion complex via acatenin. J Cell Biol 130:67–77.CrossRefGoogle Scholar
Trolice, MP, Pappalardo, A, Peluso, JJ. 1997. Basic fibroblast growth factor and N-Cadherin maintain rat granulosa cell and ovarian surface epithelial cell viability by stimulating the tyrosine phosphorylation of the fibroblast growth factor receptors. Endocrinology 138:107–13.CrossRefGoogle ScholarPubMed
Fewtrell, C. 1993. Ca+ oscillations in non-excitable cells. Annu Rev Physiol 55:427–54.CrossRefGoogle Scholar
Peluso, JJ. 1997. Putative mechanism through which N-Cadherin-mediated cell contact maintains calcium homeostasis and thereby prevents ovarian cells from undergoing apoptosis. Biochem Pharmacol 54:847–53.CrossRefGoogle ScholarPubMed
Peluso, JJ, Pappalardo, A, Fernandez, G. 2001. E-Cadherin-mediated cell contact prevents apoptosis of spontaneously immortalized granulosa cells by regulating Akt kinase activity. Biol Reprod 65:94–101.CrossRefGoogle Scholar

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