Endocrine Regulation of Menstruation

Abstract

In women, endometrial morphology and function undergo characteristic changes every menstrual cycle. These changes are crucial for perpetuation of the species and are orchestrated to prepare the endometrium for implantation of a conceptus. In the absence of pregnancy, the human endometrium is sloughed off at menstruation over a period of a few days. Tissue repair, growth, angiogenesis, differentiation, and receptivity ensue to prepare the endometrium for implantation in the next cycle. Ovarian sex steroids through interaction with different cognate nuclear receptors regulate the expression of a cascade of local factors within the endometrium that act in an autocrine/paracrine and even intracrine manner. Such interactions initiate complex events within the endometrium that are crucial for implantation and, in the absence thereof, normal menstruation. A clearer understanding of regulation of normal endometrial function will provide an insight into causes of menstrual dysfunction such as menorrhagia (heavy menstrual bleeding) and dysmenorrhea (painful periods). The molecular pathways that precipitate these pathologies remain largely undefined. Future research efforts to provide greater insight into these pathways will lead to the development of novel drugs that would target identified aberrations in expression and/or of local uterine factors that are crucial for normal endometrial function.

Adrenomedullin and its receptor, calcitonin receptor-like receptor, are aberrantly expressed in women with idiopathic menorrhagia

“…This increased expression may lead to heightened sensitivity to AM and to the production of prostaglandins, agents known to be involved in menstrual bleeding (22,23) and endometrial growth (24).…”

A review on haematological profile in menstruating, pre-menopausal and menopausal women

“…The first effect id decreased stimulation of the endometrial cells by these two hormones, followed rapidly by involution of the endometrium itself to about 65 percent of its previous thickness. Then, during the 24 hours preceding the onset of menstruation, the tortuous blood vessels leading to the mucosal layers of the endometrium become vasospastic, presumably because of some effect of involution, such as release of a vasoconstrictor material-possibly one of the vasoconstrictor types of prostaglandins that are present in abundance at this time (Jabbour et al, 2006).…”

“…They are synthesized in the ovaries, mainly from the blood but also to a slight extent from acetyl coenzyme A, multiple molecules of which can combine to form the appropriate steroid nucleus (Jabbour et al, 2006). During synthesis, mainly progesterone and androgen (testosterone and androstenedione) are synthesized first; then, during the follicular phase of the ovarian cycle stimulated by the FSH, before these two initial hormones can leave the ovaries, almost all the androgens and much of the progesterone are converted into estrogens by the enzyme aromatase in the granulosa cells.…”

Immunoprofiling of human uterine mast cells identifies three phenotypes and expression of ERβ and glucocorticoid receptor

“…In the absence of embryo implantation, the upper functional layer of the endometrium breaks down and is shed at menstruation, which is considered to bear the hallmarks of an inflammatory process ( Jabbour et al ., 2006). Endometrial tissue adjacent to the myometrium (basal compartment) is not shed during menstruation and is implicated in the rapid re-epithelialisation, cessation of bleeding and restoration of tissue homeostasis facilitating regeneration of the functional layer.…”