Hormonal regulation and bioactive substances
Preparation of the reproductive system for placental formation begins in the ovaries. During the follicular maturation phase, estrogen secretion predominates. Following ovulation, the corpus luteum forms, and its cells actively secrete progesterone. Meanwhile, androgen levels—synthesized by ovarian interstitial and theca cells—remain constant throughout the menstrual cycle.
In addition to classical steroids, the ovaries secrete a spectrum of bioactive compounds: prostaglandins, vasopressin, oxytocin, and relaxin. Growth factors (epidermal, as well as insulin-like growth factors 1 and 2) play a vital role by driving granulosa cell proliferation, follicular growth, and the selection of the dominant follicle.
Ovulation itself occurs against the backdrop of a peak surge in estrogen levels. The physical rupture of the follicular wall is mediated by prostaglandins (F₂ₐ and E₂), proteolytic enzymes within the follicular fluid, collagenase, as well as oxytocin and relaxin.
Mechanism of action and target organs
Sex hormones affect not only the uterus and mammary glands, but also numerous other tissues bearing corresponding receptors. Target organs include the brain, spongy bone tissue, the skin and its appendages (sebaceous glands, hair follicles), and the cardiovascular system (myocardium, endothelium, and vascular smooth muscle cells).
At the cellular level, interaction occurs in stages. First, the steroid hormone crosses the target cell membrane and binds to a specific cytosolic receptor (which are strictly specific for estrogens, testosterone, or progesterone). The resulting hormone-receptor complex then translocates into the cell nucleus, where it binds to chromatin and initiates the synthesis of specific proteins via DNA and RNA. Nuclear receptors also exist that can act as acceptors not only for steroids, but also for aminopeptides, glucagon, and insulin.
Systemic effects of sex steroids
The hormonal background exerts a complex systemic influence on the female body:
- Skin: Estradiol and testosterone stimulate collagen synthesis. Excess androgens lead to acne, increased skin porosity, folliculitis, and hirsutism.
- Bone tissue: Estrogens, androgens, and progesterone maintain normal bone remodeling and prevent bone resorption.
- Metabolism: The balance of steroids determines adipose tissue distribution.
- CNS: Receptors in the hippocampus and autonomic centers underlie the "menstrual wave" phenomenon—a premenstrual imbalance between inhibitory and excitatory processes in the cerebral cortex. Externally, this manifests as mild irritability and mood swings. Progesterone also actively modulates the thermoregulatory center in the hypothalamus.
Cyclic endometrial changes
For successful embryo implantation and subsequent placental development, the endometrium undergoes two sequential phases.
Immediately after menstruation, the uterine cavity is lined by only a thin basal layer measuring 1–2 mm in thickness. Its glands are short and narrow, lined with a low columnar epithelium. It is from the cells of this layer that the functional layer regenerates.
Under the predominant influence of estrogens, the proliferative phase begins, lasting 12–14 days. Epithelial cells increase in height, transitioning from a single-layered to a pseudostratified structure by the time of ovulation. The glands become tortuous and elongate, and the number of mitoses in the tissue increases. The stroma loosens and becomes edematous, with an increase in the cytoplasmic and nuclear volume of the cells. The mucosal thickness reaches 8 mm. Interestingly, the endometrium can synthesize its own estrogens from testosterone and androstenedione via the enzyme aromatase, locally enhancing proliferation.
Following ovulation, the secretory phase commences. The number of estrogen receptors declines, proliferation is halted, and progesterone takes center stage. Glycogen-containing vacuoles appear within the cells, and the glands produce a secretion rich in glycoproteins and glycosaminoglycans. The functional layer is clearly demarcated into a compact superficial layer and a spongy (spongiosa) layer.
Decidual reaction and implantation window
The optimal conditions for embryonic implantation—the so-called implantation window—are established on days 6–7 post-ovulation (corresponding to days 20–21 of a standard cycle).
Starting on day 21, a decidual reaction is triggered in the endometrial stroma, structurally resembling pregnancy-associated changes. By day 26, this reaction reaches its peak: a massive accumulation of glycogen-rich cells forms within the mucosa. These decidual cells play a pivotal role in facilitating trophoblast invasion, laying the foundation for future placental development.
To memorize the endometrial phases and their corresponding hormones, use the rule "EP": Proliferation — Estrogens, Secretion — Progesterone. First, you build the "house" (proliferation), then you fill it with "food" (glycogen secretion).
Class and exam questions
How does the endometrium regenerate following menstruation?
Glandular and stromal regeneration originates from the cells of the thin basal layer (1–2 mm) that remains in the uterine cavity following the shedding of the functional layer.
What is the "menstrual wave" phenomenon?
These are physiological changes occurring in the premenstrual days, driven by the action of steroids on the CNS. They manifest as mood swings, mild irritability, and alterations in autonomic nervous system tone.
What is the role of aromatase in the endometrium?
This enzyme enables the uterine mucosa to locally synthesize its own estrogens from testosterone and androstenedione, thereby further stimulating the proliferative process.
What else to study on this topic
- Mechanism of action of cytosolic and nuclear steroid receptors
- The role of prostaglandins, oxytocin, and relaxin in the ovulation process
- The impact of growth factors (epidermal, insulin-like) on follicular maturation
- Morphological differences between the superficial and spongy layers of the endometrium
- Changes in spiral arteries during the secretory phase of the cycle
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