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Summation of Basic Endocrine Data
Published in George H. Gass, Harold M. Kaplan, Handbook of Endocrinology, 2020
Estrogens are secreted by precursors of the follicular cells called granulosa cells and by another layer of follicular cells called the theca interna. Another source, of lesser importance, is the adrenal cortex.
Immunopathology
Published in Constantin A. Bona, Francisco A. Bonilla, Textbook of Immunology, 2019
Constantin A. Bona, Francisco A. Bonilla
Several other pathological processes may have an organ-specific autoantibody component. The syndrome known as anti-tubular basement membrane (anti-TBM) antibody disease (also called tubulointerstitial nephritis) is an inflammation of the proximal renal tubular interstitium whose origin is described in its name. Vitiligo is the depigmentation of large irregular patches of skin. Autoimmunity is strongly suspected since antibodies against melanocytes have been detected in patients. In primary ovarian failure, amenorrhea due to cessation of ovarian steroid synthesis may be caused by antibodies reactive to the theca interna of ovarian follicles.
Optimizing endometrial receptivity for patients with recurrent implantation failure
Published in Efstratios M. Kolibianakis, Christos A. Venetis, Recurrent Implantation Failure, 2019
Christos A. Venetis, Julia K. Bosdou, Efstratios M. Kolibianakis
This increase in serum progesterone was initially considered to be consistent with premature luteinization, which requires a luteinizing hormone (LH) rise or surge, which, in turn, stimulates the theca interna to produce progesterone and/or also luteinizes the existing follicles. However, through a number of studies, it was clearly shown that even in cases where LH is suppressed using gonadotrophin releasing hormone (GnRH) analogues or the oral contraceptive pill, a rise in serum progesterone is still observed.13–15 Although this led initially to the conclusion that the adrenal glands were the main source of the progesterone rise during the follicular phase, a subsequent study in which the adrenals were suppressed using dexamethasone strongly suggested that the progesterone rise is actually associated with the exogenous administration of gonadotrophins.18
Evaluation of CD4+CD25+FOXP3+ regulatory T cells and FOXP3 mRNA in premature ovarian insufficiency
Published in Climacteric, 2020
J. Xiong, R. Tan, W. Wang, H. Wang, D. Pu, J. Wu
Premature ovarian insufficiency (POI) is clinically defined as 4–6 months of amenorrhea with elevated gonadotropins and low estrogen levels, and POI affects approximately 1% of women before the age of 40 years. It presents a highly heterogeneous clinical phenotype and etiology. Genetic, iatrogenic, and autoimmune factors are potential causes of POI1. Autoimmunity is responsible for approximately 4–30% of POI cases. Accumulative evidence indicates that POI is associated with alterations in cellular immunity and humoral immunity. These alterations may include abnormal T and B lymphocyte activation2, disruptions in cytokines3, and the production of various autoantibodies, such as adrenal cortex autoantibody (AAA)4. The prevalence of associated clinical autoimmune diseases in POI patients varies between 10 and 55%, with thyroid disorders representing the most common of these diseases, being detected in 12–40% of patients5. The histopathological analysis of ovaries from women with POI reveals the infiltration of CD4+ and CD8+ T lymphocytes and plasma cells into the theca interna and externa layers of the follicle and within the corpus luteum, and, occasionally, the granulosa cell layer is also involved6. However, the contribution of autoimmune deregulation to the pathogenesis of ovarian follicle depletion and dysfunction remains elusive.
Effect of resistin on estradiol and progesterone secretion from human luteinized granulosa cells in culture
Published in Systems Biology in Reproductive Medicine, 2019
Christina I. Messini, Anna Vasilaki, Evangelia Korona, George Anifandis, Panagiotis Georgoulias, Konstantinos Dafopoulos, Antonios Garas, Alexandros Daponte, Ioannis E. Messinis
Information regarding the role of resistin in the regulation of ovarian steroidogenesis in humans is limited. There are only two studies; in the first, theca interna cells were obtained from the ovaries of two regularly cycling premenopausal women during hysterectomy (Munir et al. 2005). In agreement with data in pigs (Rak- Mardyla et al. 2013), it was shown that in a 3-day culture of the theca cells resistin enhanced the expression of 17α-hydroxylase activity only in the presence of forskolin or forskolin combined with insulin (Munir et al. 2005). In the second study, granulosa cells were obtained from women undergoing IVF/ICSI treatment (Reverchon et al. 2013). It was shown that resistin did not affect basal estradiol and progesterone secretion in the presence or in the absence of FSH, but it eliminated the IGF1-stimulated secretion of these steroids. In that study, only a single dose of 10 ng/ml resistin was used and therefore it is not known what higher or lower dosages would do. It is evident that there is no consistency between the animal and the human data, while information in humans regarding the effect of resistin on ovarian steroidogenesis is scant.
From a circle to a sphere: the ultrasound imaging of ovarian follicle with 2D and 3D technology
Published in Gynecological Endocrinology, 2019
Claudia Re, Mario Mignini Renzini, Amelia Rodriguez, Mariabeatrice Dal Canto, Matteo Buccheri, Sandro Sacchi, Silvia Bartolucci, Rubens Fadini, Antonio La Marca
Primordial follicles are quiescent until a balance between the growing and apoptotic factors promotes the exit from a quiescent status. The age related depletion of primordial follicles occurs as a result of two processes: atresia and entry in the growth phase: until the age of 30, the loss of primordial follicles is due to atresia, after, this loss is due to the entrance in the growth phase. The activation of primordial to primary follicles includes some changes in granulose cells (proliferation and differentiation) and the zona pellucida appearance so that the oocyte is covered and separated from granulosa cells by a glycoprotein polymer capsule. When transforming into secondary follicles, the external layer cells that covered the outer layer of the follicle, become theca externa and theca interna, following a cyto-differentiation. Finally, the formation of a fluid-filled cavity, adjacent to the oocyte and called antrum, defines the antral or tertiary follicle.