Female Reproductive Function

Author(s):  
Sergio R. Ojeda

The production of germ cells is essential for the continuation of a species. In the female this function is accomplished by the ovaries. In addition, the ovaries secrete steroids and nonsteroidal hormones that not only regulate the secretion of anterior pituitary hormones but also act on various target organs, including the ovaries themselves, the uterus, fallopian tubes, vagina, mammary gland, and bone. Morphologically, the ovary has three regions: an outer cortex that contains the oocytes and represents most of the mass of the ovary; the inner medulla, formed by stromal cells and cells with steroid-producing characteristics; and the hilum, which, in addition to serving as the point of entry of the nerves and blood vessels, represents the attachment region of the gland to the mesovarium. The cortex, which is enveloped by the germinal epithelium, contains the follicles, which are the functional units of the ovary. They are present in different states of development or degeneration (atresia), each enclosing an oocyte. In addition to the oocyte, ovarian follicles have two other cellular components: granulosa cells, which surround the oocyte, and thecal cells, which are separated from the granulosa cells by a basal membrane and are arranged in concentric layers around this membrane. The follicles are embedded in the stroma, which is composed of supportive connective cells similar to that of other tissues, interstitial secretory cells, and neurovascular elements. The medulla has a heterogeneous population of cells, some of which are morphologically similar to the Leydig cells in the testes. These cells predominate in the ovarian hilum; their neoplastic transformation results in excess androgen production. The ovary produces both steroids and peptidergic hormones. Whereas the steroids are synthesized in both interstitial and follicular cells, peptidergic hormones are primarily produced in follicular cells and, after ovulation, by cells of the corpus luteum. The initial precursor for steroid biosynthesis is cholesterol, which derives from animal fats of the diet or from local synthesis.

Author(s):  
Mikhail S. Shelygin ◽  
Nadezhda S. Guziy ◽  
Viktoria S. Kaplitskaya

The combined dyshormonal pathology of the uterus and mammary glands represents a great danger to the health of a woman, as well as impairs the quality of life, reduces the reproductive capacity of a woman and leads to premature loss of reproductive function. Steroid hormones play a large role in the regulation of proliferative changes in the uterus and mammary glands. Regulation of target organs, uterus and mammary glands, due to the presence of common mechanisms associated with the presence of the receptor apparatus in the tissues of these organs to sex hormones. The general links of pathogenesis and the high frequency of combined pathology of the uterus and mammary glands are of interest to study not only isolated forms of proliferation, but also the development of a unified systematic approach to the study of this pathology. In recent times, there are opposing views on the role of hormonal dysfunction as a factor in proliferative processes. The management tactics of patients with pathological changes in the mammary gland in various gynecological diseases is an assessment of endocrine status, normalization of hormonal and metabolic disorders, especially when progesterone and cortisol are excreted, testosterone levels are increased, and hyperprolactinemia is affected. Special attention should be paid to patients with menstrual disorders, reproductive health disorders. We believe that the problem of the hyperproliferative processes of the uterus and mammary glands should not be considered only from the perspective of gynecological or mammological practice. This pathology is polymorphic and should have broad interdisciplinary connections with such disciplines as oncology, endocrinology, gastroenterology, psychiatry, therapy, pathomorphology, histology, obstetrics and gynecology. Only by studying all possible links of etiopathogenesis, by combining interdisciplinary communication, it is possible to effectively fight for the quality of patients with a combined pathology of the uterus and mammary glands. Family planning, prevention of unplanned pregnancy, timely implementation of maternity, prevention of miscarriage, the use of modern contraceptives, support for breastfeeding is also of high importance for the prevention of disorders and the preservation, extension of reproductive capabilities, and the prevention of combined dyshormonal pathology of the uterus and breast.


2005 ◽  
Vol 230 (5) ◽  
pp. 292-306 ◽  
Author(s):  
Shabrine S. Daftary ◽  
Andrea C. Gore

Given the close relationship among neuroendocrine systems, it Is likely that there may be common signals that coordinate the acquisition of adult reproductive function with other homeo-static processes. In this review, we focus on central nervous system insulin-like growth factor-1 (IGF-1) as a signal controlling reproductive function, with possible links to somatic growth, particularly during puberty. In vertebrates, the appropriate neurosecretion of the decapeptide gonadotropin-releas-ing hormone (GnRH) plays a critical role in the progression of puberty. Gonadotropin-releasing hormone is released in pulses from neuroterminals in the median eminence (ME), and each GnRH pulse triggers the production of the gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone (FSH). These pituitary hormones in turn stimulate the synthesis and release of sex steroids by the gonads. Any factor that affects GnRH or gonadotropin pulsatility is important for puberty and reproductive function and, among these factors, the neurotrophic factor IGF-1 is a strong candidate. Although IGF-1 is most commonly studied as the tertiary peripheral hormone in the somatotropic axis via its synthesis in the liver, IGF-1 Is also synthesIzed in the brain, within neurons and glia. In neuroendocrine brain regions, central IGF-1 plays roles in the regulation of neuroendocrine functions, including direct actions on GnRH neurons. Moreover, GnRH neurons themselves co-express IGF-1 and the IGF-1 receptor, and this expression is developmentally regulated. Here, we examine the role of IGF-1 acting in the hypothalamus as a critical link between reproductive and other neuroendocrine functions.


1973 ◽  
Vol 59 (2) ◽  
pp. 353-361
Author(s):  
NATALIE POURREAU-SCHNEIDER

SUMMARY An androgen-producing testicular interstitial cell tumour of rats was grafted into intact and spayed female rats. The tumour inhibited luteinization, produced follicular atresia, stimulated the uterine myometrium and endometrium, and caused vaginal mucus formation. Anoestrus set in and mating behaviour disappeared, rendering gestation impossible. After surgical removal of the tumour, the masculinization disappeared rapidly. With the return of vaginal oestrus (sometimes only 4 days after removal of the tumour) most of the rats mated and gave birth to normal young. When a palpable nodule reappeared, the reproductive function was again lost. The tumour produced similar changes in the target organs of spayed females. The inhibitory action of the endocrine tumour on pituitary gonadotrophic hormone production was shown by the absence of castration cells in the pituitary of the tumour-bearing spayed female.


1998 ◽  
Vol 76 (1) ◽  
pp. 27-35 ◽  
Author(s):  
Jie Pan ◽  
Nelly Auersperg

Ovarian granulosa cells are derived embryologically from two keratin-positive epithelia of mesodermal origin, the ovarian rete and the ovarian surface epithelium. In the rat, presumptive granulosa cells still express keratin at birth but as they acquire functions related to oocyte support and steroidogenesis in the maturing ovary they lose this epithelial differentiation marker. Using double-label immunofluorescence microscopy, we examined the distribution of keratin-expressing granulosa cells in rat ovaries on days 1-10 postpartum in relation to (i) laminin and collagen type IV in follicular basement membranes, (ii) the zona pellucida, and (iii) 3β-hydroxysteroid dehydrogenase activity. Keratin was present in most (pre)granulosa cells on days 1-3. As the cells became multilayered in growing follicles, keratin was retained by granulosa cells adjacent to follicular basement membranes but disappeared from cells that were displaced towards follicular centers. From day 7 on, large follicles lacked keratin altogether. Laminin was a consistent component of follicular basement membranes at all ages, while collagen IV varied and diminished in parallel with keratin. 3β-Hydroxysteroid dehydrogenase was demonstrable in stromal interstitial cells from day 7 on. Zona pellucida first appeared in primary follicles adjacent to keratin-positive cells and subsequently became surounded with keratin-negative granulosa cells in growing follicles. The results suggest different roles for laminin and collagen IV in follicular basement membranes and support the hypothesis that keratin expression by granulosa cells depends on paracrine interactions with the ovarian stroma. In early growing follicles, these interactions may be interrupted by physical removal from the vicinity of the basement membranes as the granulosa cells become multilayered. In the more mature follicles, the loss of keratin from all granulosa cells suggests that the required stromal signals cease, perhaps as the perifollicular stroma differentiates into the theca.Key words: ovary, differentiation, keratin, basal membrane, development.


2020 ◽  
Vol 10 (4-s) ◽  
pp. 142-147
Author(s):  
ZINE CHARAF KHALLOUA ◽  
IMENE CHEBLI ◽  
SAMIRA MEZIANI ◽  
DALILA FERRAG ◽  
AMINA ITATAHINE ◽  
...  

Background: In last few years .; it’s  increasingly being recognized  that  Reproductive function is controlled by the hypothalamic–pituitary– gonadal axis, which is regulated by numerous endogenous and environmental factors  such us adipose accumulation in obesity  contributing to reproductive failure  such as menstrual disorders and infertility, gestational failure and obstetric complications, and infertility , Distinct changes in circulating sex hormones appear to underline these abnormalities. The objective: The aim of this study was to elucidate the possible correlation between body mass index as fatness indicator and hormonal profile in infertile women from the west of Algeria. To identify the impact of overweight  and obesity on female hormonal profile ; we  conducted a prospective study  measuring pituitary hormones  (FSH  and LH and prolactin ) , steroid sex hormones ( progesterone , testosterone and estradiol ) , anti miulleian hormone , and thyroidal hormones (FT3 , FT4 and TSH) in 360 women  consulting for subfertility in private genecologycal and obstetrical centers in SID BELABESS (West of Algeria ) Result: Our study showed that the majority of patients were aged between 20 and 29 years, representing a percentage of 47.8%, with the average age in sample (31.65 ± 6,93ans). The majority of subjects was obese   46.4%, or overweight (39.4%) with an average BMI of (29.76 ± 4,85Kg / m2). No statistically significant association was found between the BMI as obesity indicator with hormonal levels of pituitary hormones  (FSH  and LH and prolactin ) , steroid sex hormones ( progesterone , testosterone and estradiol ) , anti miulleian hormone , and thyroidal hormones (FT3 , FT4 and TSH). A negative and statistically significant correlation between the age of the patients and the AMH level (R = -0.60, P <0.01) was noted. Conclusion: The results of our study showed that the majority of women included in our study had a high BMI but no statistical significant difference was found between underweight , normal , overweight and obese women , that’s why more studies should be conducted to elucidate the in which level does obesity impair the reproductive outcomes. Keywords: Female infertility, hormonal profile, BMI, SBA, Algeria.


2021 ◽  
Vol 51 (3) ◽  
pp. 41-43
Author(s):  
V. I. Kulakov ◽  
А. S. Gasparov ◽  
T. А. Nazarenko

Endometnosis is not a disease of individual organs and systems, but of the whole organism, the treatment of which requires complex action. The effect of all drugs used to treat endometriosis is to suppress growth factors and the development of pathological implants at different levels of the system - from the hypothalamus to target organs. The problem of restoring reproductive function in patients with endometriosis-associated infertility remains very urgent at the present time. This is due to the prevalence of this pathological process - in the structure of female infertility, endometriosis is about 50%.


2020 ◽  
Vol 103 (3) ◽  
pp. 583-598
Author(s):  
Patricia G Tremblay ◽  
Marc-André Sirard

Abstract The female reproductive function largely depends on timing and coordination between follicle-stimulating hormone (FSH) and luteinizing hormone. Even though it was suggested that these hormones act on granulosa cells via shared signaling pathways, mainly protein kinases A, B, and C (PKA, PKB, and PKC), there is still very little information available on how these signaling pathways are regulated by each hormone to provide such differences in gene expression throughout folliculogenesis. To obtain a global picture of the principal upstream factors involved in PKA, PKB, and PKC signaling in granulosa cells, human granulosa-like tumor cells (KGN) were treated with FSH or specific activators (forskolin, SC79, and phorbol 12-myristate 13-acetate) for each pathway to analyze gene expression with RNA-seq technology. Normalization and cutoffs (FC 1.5, P ≤ 0.05) revealed 3864 differentially expressed genes between treatments. Analysis of major upstream regulators showed that PKA is a master kinase of early cell differentiation as its activation resulted in the gene expression profile that accompanies granulosa cell differentiation. Our data also revealed that the activation of PKC in granulosa cells is also a strong differentiation signal that could control “advanced” differentiation in granulosa cells and the inflammatory cascade that occurs in the dominant follicle. According to our results, PKB activation provides support for PKA-stimulated gene expression and is also involved in granulosa cell survival throughout follicular development. Taken together, our results provide new information on PKA, PKB, and PKC signaling pathways and their roles in stimulating a follicle at the crossroad between maturation/ovulation and atresia.


Endocrinology ◽  
2002 ◽  
Vol 143 (8) ◽  
pp. 3071-3082 ◽  
Author(s):  
Ganesan Sathya ◽  
Michelle S. Jansen ◽  
Susan C. Nagel ◽  
C. Edgar Cook ◽  
Donald P. McDonnell

Abstract The steroid hormones estrogen and progesterone together regulate the development and maintenance of the female reproductive system. The actions of these two hormones are mediated by their respective nuclear receptors located within overlapping cell populations in target organs. The molecular mechanism of action of these two hormones has been defined to a large extent using estrogen receptor (ER) and progesterone receptor (PR) antagonists. In the case of ER, the available antagonists are highly receptor selective. With respect to PR, however, the available antiprogestins also interact with the receptors for glucocorticoids, mineralocorticoids, and androgens. Whereas these cross-reactivities can usually be managed in studies of female reproductive function, it is the recent demonstration that RU486 is an effective antagonist of the β-isoform of ER that suggested the need for more selective antiprogestins. In this study, we used cell-based transcriptional assays combined with screens using coactivator peptide analogs to identify two novel classes of antiprogestins that distinguish themselves from the antiprogestin RU486 in the manner they interact with PR. One class exhibits the characteristics of a pure antiprogestin in that its members bind to the receptor and induce a conformational change that prevents the presentation of two potential coactivator binding surfaces on the protein. The second class of compounds distinguish themselves from RU486 in that they are ERβ sparing. When tested in vivo the ER-sparing antiprogestins were as effective as RU486 in suppressing superovulation. It is anticipated that the availability of these new antiprogestins will advance the studies of PR pharmacology in a manner similar to how the availability of selective ER modulators has helped the study of ER action.


1971 ◽  
Vol 103 (8) ◽  
pp. 1063-1078 ◽  
Author(s):  
Petr Masner ◽  
Vladimir Landa

AbstractOvaries are one of the target organs hit by the nucleic acid antimetabolite 6-azauridine. All the malformations observed are caused by the suppression of mitotic activity, which appears to be the most sensitive to the applied drug. The inhibition of mitosis in the apical trophocytes results in depletion of the nutritive tissue in older females, followed by a disturbance of previtellogenesis and activation of oocytes. The blocked mitotic multiplication of prefollicular tissue results in exhaustion of this layer followed by a disturbance of regular egg chamber formation. The inadequate separation of oocytes by follicular cells causes the arrangement of the oocytes in paired chambers, often blocking the ovariole, or the formation of compound chambers. The oocytes sharing the compound chamber either remain separated by the ooplasmalemma or merge. Eggs with adherent dwarf oocytes or giant fused double eggs are oviposited. Endomitotic DNA replication and amitotic karyokinesis of the follicular cells are not interfered with by 6-azauridine, probably owing to the nucleic acid pools contained in the haemolymph. The lecytholitic cells resorb the ooplasm utilizing the nucleic acid-rich material.


Reproduction ◽  
2014 ◽  
Vol 147 (2) ◽  
pp. 221-229 ◽  
Author(s):  
Lisa Dupuis ◽  
Yasmin Schuermann ◽  
Tamara Cohen ◽  
Dayananda Siddappa ◽  
Anitha Kalaiselvanraja ◽  
...  

Leptin is an important hormone influencing reproductive function. However, the mechanisms underpinning the role of leptin in the regulation of reproduction remain to be completely deciphered. In this study, our objective is to understand the mechanisms regulating the expression of leptin receptor (Lepr) and its role in ovarian granulosa cells during ovulation. First, granulosa cells were collected from superovulated mice to profile mRNA expression of Lepr isoforms (LeprA and LeprB) throughout follicular development. Expression of LeprA and LeprB was dramatically induced in the granulosa cells of ovulating follicles at 4 h after human chorionic gonadotropin (hCG) treatment. Relative abundance of both mRNA and protein of CCAAT/enhancer-binding protein β (Cebpβ) increased in granulosa cells from 1 to 7 h post-hCG. Furthermore, chromatin immunoprecipitation assay confirmed the recruitment of Cebpβ to Lepr promoter. Thus, hCG-induced transcription of Lepr appears to be regulated by Cebpβ, which led us to hypothesise that Lepr may play a role during ovulation. To test this hypothesis, we used a recently developed pegylated superactive mouse leptin antagonist (PEG-SMLA) to inhibit Lepr signalling during ovulation. I.p. administration of PEG-SMLA (10 μg/g) to superovulated mice reduced ovulation rate by 65% compared with control treatment. Although the maturation stage of the ovulated oocytes remained unaltered, ovulation genes Ptgs2 and Has2 were downregulated in PEG-SMLA-treated mice compared with control mice. These results demonstrate that Lepr is dramatically induced in the granulosa cells of ovulating follicles and this induction of Lepr expression requires the transcription factor Cebpβ. Lepr plays a critical role in the process of ovulation by regulating, at least in part, the expression of the important genes involved in the preovulatory maturation of follicles.


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