scholarly journals Survival of Human Ovarian Follicles from Fetal to Adult Life: Apoptosis, Apoptosis-Related Proteins, and Transcription Factor GATA-41

2001 ◽  
Vol 86 (7) ◽  
pp. 3421-3429 ◽  
Author(s):  
Tommi E. Vaskivuo ◽  
Mikko Anttonen ◽  
Riitta Herva ◽  
Håkan Billig ◽  
Marinus Dorland ◽  
...  

The majority of oocytes present in fetal ovaries are depleted before birth, and only about 400 will ovulate during the normal fertile life span. Studies on animals have shown that apoptosis is the mechanism behind oocyte depletion and follicular atresia. In the present study, we investigated the extent and localization of apoptosis in human fetal (aged 13–40 weeks) and adult ovaries. Furthermore, the expression of apoptosis-regulating proteins, bcl-2 and bax, and the relationship of transcription factor GATA-4 were studied. Apoptosis was found in ovarian follicles throughout fetal and adult life. During fetal development, apoptosis was localized mainly to primary oocytes and was highest between weeks 14–28, decreasing thereafter toward term. Expression of bcl-2 was observed only in the youngest fetal ovaries (weeks 13–14), and bax was present in the ovaries throughout the entire fetal period. In adult ovaries, apoptosis was detected in granulosa cells of secondary and antral follicles, and Bcl-2 and bax were expressed from primary follicles onwards. During fetal ovarian development, GATA-4 messenger RNA and protein were localized to the granulosa cells, with expression being highest in the youngest ovaries and decreasing somewhat toward term. The expression pattern of GATA-4 suggests that it may be involved in the mechanisms protecting granulosa cells from apoptosis from fetal to adult life. The results indicate that depletion of ovarian follicles in the human fetus occurs through intrinsic mechanisms of apoptosis in oocytes, and later in adult life the survival of growing follicles may be primarily determined by granulosa cell apoptosis.

2009 ◽  
Vol 81 (Suppl_1) ◽  
pp. 378-378 ◽  
Author(s):  
Ken Taniguchi ◽  
Toshiaki Taketani ◽  
Lifa Merry Lee ◽  
Fumie Kizuka ◽  
Isao Tamura ◽  
...  

2005 ◽  
Vol 90 (6) ◽  
pp. 3752-3756 ◽  
Author(s):  
Tommi E. Vaskivuo ◽  
Minna Mäentausta ◽  
Svea Törn ◽  
Olayiwola Oduwole ◽  
Annika Lönnberg ◽  
...  

Estrogen action plays a crucial role in many processes throughout the human life span, including development. Estrogens are pivotal in the regulation of female reproduction, but little is known about their role during ovarian development. To better understand estrogen action during ovarian development, the expression of estrogen receptors (ERs)-α and -β and key enzymes regulating estradiol production, 17β-hydroxysteroid dehydrogenases (17HSDs) types 1, 2, and 7, were analyzed in human fetal ovaries. The expression of ERs was related to the development of ovarian follicles. Before the 26th week of fetal life ERα was only occasionally detected, but from then onward, its expression was detected in ovarian follicles. Consistent expression of ERβ was seen from the 20th week until term. Both ERα and ERβ were localized to the granulosa cells and oocytes. Expression of 17HSD1 and 17HSD7 enzymes, catalyzing the conversion of estrone to more active estradiol, was detected as early as at the 17th week of fetal life. The expression of 17HSD1 displayed a pattern similar to that of ERs and increased toward term, whereas that of 17HSD7 decreased and was negative by the 36th week. 17HSD1 was localized to the granulosa cells, whereas 17HSD7 expression was more diffuse and was found in both granulosa and stromal cells. 17HSD2, converting estradiol to less potent estrone, was negative in all samples studied. The simultaneous appearance of estrogen-converting enzymes and ERs at the time of follicle formation indicates that the machinery for estrogen action exists in fetal ovaries and suggests a possible role for estrogens in the developing ovary.


1992 ◽  
Vol 4 (3) ◽  
pp. 433-449 ◽  
Author(s):  
Antonia Bifulco ◽  
Tirrill Harris ◽  
George W. Brown

AbstractTwo population enquiries in Walthamstow and Islington, London, have shown that loss of the mother before the age of 17 years, either by death or separation for a year or more, doubles the risk of depressive and anxiety disorders among adult women. Furthermore, there was a particularly high rate of adult depression among those whose mothers died before they were 6 years old, and this was associated with a measure of childhood helplessness. There was no such link of either adult disorder or childhood helplessness with age at loss under 6 years for those losing a mother by separation. Two possible explanations were explored for these contrasting results. That concerning the adequacy of mourning of the mother's death received no support. However, evidence indicated that experience with the mother before the loss (usually affected by ongoing illness) explained the link of adult depression or anxiety with her early death. The failure of age at loss to relate in the separation group was probably due to the fact that among them age of separation was not a good indication of the quality of maternal care before age 6. Indirect evidence emerged which suggested that quality of early attachment (before age 6) to the natural mother before any loss relates to childhood helplessness. This in turn relates to a higher risk of disorder in adult life.


Development ◽  
2001 ◽  
Vol 128 (1) ◽  
pp. 125-135 ◽  
Author(s):  
J.F. Reiter ◽  
Y. Kikuchi ◽  
D.Y. Stainier

Previous studies have indicated that gata5, a zinc-finger transcription factor gene, is required for the development of the zebrafish gut tube. Here, we show that gata5 mutants also display defects in the development of other endodermal organs such as the liver, pancreas, thyroid and thymus. gata5 is expressed in the endodermal progenitors from late blastula stages, suggesting that it functions early during endoderm development. We indeed find that during gastrulation stages, gata5 mutants form fewer endodermal cells than their wild-type siblings. In addition, the endodermal cells that form in gata5 mutants appear to express lower than wild-type levels of endodermal genes such as sox17 and axial/foxA2. Conversely, overexpression of gata5 leads to expanded endodermal gene expression. These data indicate that Gata5 is involved both in the generation of endodermal cells at late blastula stages and in the maintenance of endodermal sox17 expression during gastrulation. We have also analyzed the relationship of Gata5 to other factors involved in endoderm formation. Using complementary mutant and overexpression analyses, we show that Gata5 regulates endoderm formation in cooperation with the Mix-type transcription factor Bon, that Gata5 and Bon function downstream of Nodal signaling, and that cas function is usually required for the activity of Gata5 in endoderm formation. Finally, we show that fau/gata5, bon and cas exhibit dominant genetic interactions providing additional support that they function in the same pathway. Together, these data demonstrate that Gata5 plays multiple roles in endoderm development in zebrafish, and position Gata5 relative to other regulators of endoderm formation.


Author(s):  
N. V. Hasiuk

Background. Periodontal diseases are a topical issue of contemporary dentistry because they are accompanied by severe morphological and functional disorders of maxillodental system; and are characterized by polyetiology and a number of metabolic disorders.The purpose of this study was to substantiate the pathogenic mechanisms of generalized periodontitis in relation to polymorphism of nuclear transcription factor NF- κB1.Objective. The aim of the study was to determine the genetic factors in the development of generalized periodontitis and the relationship of this parameter with immunohistochemical affiliation for cellular infiltrate of the lamina propria of gum at this nosology in young people. Hence, 2 groups were formed: І – control and II – observational.Methods. Polymorphic gene section NF-κB1 was determined using the cells of buccal epithelium of the examined people by means of polymerase chain reaction. Collection of material was performed with sterile disposable dental brush, followed by the introduction of a reagent in ependorph with DNA Express reagent (LyTeh NPF, Russia). Genome deoxyribonucleic acid was isolated by DNA Express set (LyTeh, Moscow).Results. The lack of correlation in this case indicates that no matter how parameters change, relatively major genotype (Del/Del) in this case is unchanged and the determining factor causes the development of generalized periodontitis, clinical picture of which is rapidly progressing.Conclusions. Results of correlation analysis proved that genotype (Del/Del), as polymorphic variant of gene transcription factor NF-κB1, was significantly associated with the emergence of rapidly progressive periodontitis in young people.


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