ABSTRACT
During a woman’s reproductive years, the concerted effects of ovarian-derived estradiol (E2) and progesterone regulate the cyclical changes in the functional endometrial layer that prepare it to receive the implanting blastocyst. In the absence of implantation, the endometrium is sloughed off in the menstrual fluid. Restoration of the endometrium begins in the follicular phase of the next cycle as rising circulating E2 levels initiate cell proliferation. In the postovulatory period, rising circulating progesterone levels stimulate the E2-primed endometrial cells together with a second peak of E2 to stop proliferation and initiate differentiation. Consequently, the glands become tortuous and secrete an array of products that markedly influence the uterine milieu encountered by the implanting blastocyst. The stromal cells undergo decidualization. This process represents the sum total of morphological and biochemical changes that transform precursor stromal cells into decidual cells. The decidualization reaction is initiated around blood vessels and under the glands.1 Continued stimulation by E2 and progesterone induces the spread of decidualization throughout the luteal phase and gestational endometrium.2 An integral component of decidualization is a marked alteration in the expression of proteins that promote hemostasis and enhance vascular stability.
