he apical surface of the amnionic epithelium is replete with highly developed microvilli. This structure relects its function as a major site of transfer between amnionic luid and amnion. This epithelium is metabolically active, and its cells synthesize tissue inhibitor of MMP-l, prostaglandin E2 (PGE2), and fetal ibronectin (FN) (Rowe, 1997). Although epithelia produce FN, recent studies suggest that ibronectin functions in the underlying mesenchymal cells. Here, FN promotes synthesis of MMPs that break down the strength-bearing collagens and enhance prostaglandin synthesis to prompt uterine contractions (Mogami, 2013). This pathway is upregulated in premature rupture of membranes induced by thrombin or infection-induced release of FN (Chigusa, 2016; Mogami, 2014).
Epithelial cells may respond to signals derived from the fetus or the mother, and they are responsive to various endocrine or paracrine modulators. Examples include oxytocin and vasopressin, both of which increase PGE2 production in vitro (Moore, 1988). They may also produce cytokines such as IL-8 during labor initiation (Elliott, 2001).
Amnionic epithelium also synthesizes vasoactive pep tides, including endothelin and parathyroid hormone-related protein (Economos, 1992; Germain, 1992). he tissue produces brain natriuretic peptide (BNP) and corticotropin-releasing hormone (CRH), which are peptides that invoke smooth-muscle relaxation (Riley, 1991; Warren, 1995). BNP production is positively regulated by mechanical stretch in fetal membranes and is proposed to function in uterine quiescence. Epidermal growth factor, a negative regulator ofBNP, is up regulated in the membranes at term and leads to a decline in BNP-regulated uterine quiescence (Carvaj al, 2013). It seems reasonable that vasoactive peptides produced in amnion gain access to the adventitial surface of chorionic vessels. hus, the amnion may be involved in modulating chorionic vessel tone and blood low. Amnionderived vasoactive peptides function in both maternal and fetal tissues in diverse physiological processes. AOter their secretion, these bioactive agents enter amnionic luid and thereby are available to the fetus by swallowing and inhalation.
Mesenchymal cells of the amnionic ibroblast layer are responsible for other major functions. Synthesis of interstitial collagens that compose the compact layer of the amnion-the major source of its tensile strength-takes place in mesenchymal cells (Casey, 1996). At term the generation of cortisol by l1�-hydroxysteroid dehydrogenase may contribute to membrane rupture via reduction of collagen abundance (Mi, 2017). Mesenchymal cells also synthesize cytokines that include IL-6, IL-8, and MCP-I. Cytokine synthesis rises in response to bacterial toxins and IL-1. his functional capacity of amnion mesenchymal cells is an important consideration in amnionic fluid study of labor-associated accumulation of inlammatory mediators (Garcia-Velasco, 1999). Finally, mesenchymal cells may be a greater source of PGE2 than epithelial cells, especially in the case of premature membrane rupture (Mogami, 2013; Whittle, 2000).