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Delivery of Ovarian Hormones for Bone Health
Published in Emmanuel Opara, Controlled Drug Delivery Systems, 2020
The ovaries are part of the complex HPO axis (Figure 7.1). This system operates through the secretion of GnRH from the hypothalamus to the anterior pituitary via the hypophyseal portal system of the infundibulum,2 as triggered by upstream signals such as kisspeptin cells in the diencephalon.90 GnRH, in turn, leads to secretion of FSH and LH from the anterior pituitaries, which enter the bloodstream to reach the ovaries, where they promote secretion of estrogen, progesterone, and other hormones. The secretion of estrogen and progesterone as well as hormones, including activin, inhibin, and testosterone, from the ovaries have feedforward and feedback control mechanisms on the secretion of the hypothalamic and pituitary hormones. As such, loss of the ovarian hormones due to loss of ovarian function has systemic effects not only on target tissues, to be discussed below, but also on the hormone levels of the hypothalamic and pituitary hormones. That is, the loss or change in ovarian hormone production (e.g., estrogen and inhibin) and blood concentrations also leads to changes in plasma concentrations of the anterior pituitary hormones before, during, and after menopause.104,123 Although changes in the ovarian hormone levels affect hypothalamus and pituitary hormones, the converse is also true. Indeed, changes in plasma levels of FSH and changes in LH and GnRH are observed prior to decreases in estrogen and progesterone concentrations associated with the menopausal transition.146
High-level production and purification of bioactive recombinant human activin A in Chinese hamster ovary cells
Published in Preparative Biochemistry & Biotechnology, 2023
Changin Kim, Hyunjoo Kim, Jeong Soo Park, Jiwon Park, Jeongmin Oh, Jaeseung Yoon, Kwanghee Baek
Activins, disulfide-linked homo- and heterodimers of inhibin β subunits and member of the transforming growth factor-β (TGF-β) superfamily, were originally recognized for their capacity to induce the release of follicle-stimulating hormone (FSH).[1,2] Activin A is also a homodimer of the inhibin βΑ subunit which is one of five types of inhibin subunits described so far and is the best characterized.[3,4] Like all members of the TGF-β superfamily, activin A is initially synthesized as a large precursor polypeptide consisting of a secretory signal peptide, pro-domain, and small mature domain. During the processes that occur within the secretory pathway, the formation of a dimer by two precursor subunits occurs by way of the disulfide linkage of conserved cysteine residues located in the mature domains with recognition and cleavage of the polybasic RRRRR motif between pro- and mature domains by furin-like protease releasing a mature form of bioactive activin A.[5,6] Studies on mutagenesis of the cleavage site have suggested that the biological activity of activin A requires proteolytic cleavage between pro- and mature domains.[7] Although activin A contains one glycosylation site in its pro-domain, its biological activity and secretion are unaffected by glycosylation-deficient cases.[8]
Pre-pubertal exposure to ibuprofen impairs sperm parameters in male adult rats and compromises the next generation
Published in Journal of Toxicology and Environmental Health, Part A, 2020
Mariana Gazoli Barbosa, Bárbara Campos Jorge, Julia Stein, Dayana Agnes Santos Ferreira, Ana Carolina da Silva Barreto, Ana Carolina Casali Reis, Suyane Da Silva Moreira, Leonardo Cesar De Lima Inocencio, Luis Fernando Benitez Macorini, Arielle Cristina Arena
Previous ex vivo and in vitro studies demonstrated that ibuprofen is able to compromise genes expression involved in steroidogenesis and transport of cholesterol to mitochondria of Leydig cell (Kristensen et al. 2018). A study conducted by Ben Maamar et al. (2017) has demonstrated that the expression of at least of 3 steroidogenic enzymes (CYP11A1, CYP17A1, and HSD17B3) was suppressed in human fetal testes by ibuprofen using ex vivo culture and xenograft systems, reinforcing that ibuprofen can act as an endocrine disruptor. Thus, the reduction in testosterone levels, as well as the atrophy detected in Leydig cells nuclei of exposed males can be associated with an interference of ibuprofen in the steroidogenesis process. In contrast, FSH and LH levels were increased in adult-treated males. This increase could be explained by the negative feedback provoked by the lower circulating testosterone levels on the pituitary as well as a change in the production of inhibin by Sertoli cells. While the LH-testosterone axis regulates the androgenization, the FSH-inhibin axis is responsible for the control of sperm production (Schlatt and Ehmcke 2014).
How the quest to improve sheep reproduction provided insight into oocyte control of follicular development
Published in Journal of the Royal Society of New Zealand, 2018
Ovarian follicular growth and ovulation is controlled by complex communication among the hypothalamus, pituitary, ovary and uterus (Figure 2). The hypothalamus secretes gonadotrophin releasing hormone (GnRH), which acts on the pituitary to cause synthesis and release of the gonadotrophins, follicle stimulating hormone (FSH) and luteinising hormone (LH) (Clarke & Arbabi 2016). In turn, FSH and LH act on cells in the ovarian follicle to support its growth and maturation (Webb & Campbell 2007). Initially, FSH acts on granulosa cells to stimulate proliferation and differentiation. LH stimulates production of androstenedione from the theca that then is used as a substrate by granulosa cells to produce oestradiol. As the follicle grows, increased amounts of inhibin are also produced by the granulosa cells and, together with oestradiol, these feedback to the pituitary to inhibit FSH synthesis and release (Webb & Campbell 2007). Oestradiol, as well as progesterone produced by the corpus luteum, also inhibit GnRH release from the hypothalamus, suppressing the release of the gonadotrophins (Goodman et al. 2002). However, as the follicle continues to grow, the granulosa cells mature and they begin to express LH receptors (LHR). FSH concentrations fall during selection of the follicles that will go on to ovulation. Follicles that are mature enough to express LHR on the granulosa cells are able to survive through the additional support of LH, as FSH concentrations are suppressed. Less mature gonadotrophin dependent follicles, that have yet to express LHR on the granulosa cells, die in this environment. The mature follicles continue to grow and synthesise increasing levels of oestradiol (Webb & Campbell 2007). During the follicular phase, following the regression of the corpus luteum triggered by release of prostaglandin F2α from the uterus (Niswender et al. 2000), oestradiol reaches a critical threshold. At this stage, oestradiol actually switches from negative to positive feedback, causing the release of the preovulatory gonadotrophin surge (Caraty et al. 1995), and ovulation of the mature follicle(s) (usually one or two in sheep).