“…As evidenced by its expression of genes for many proteins, such as uterine milk proteins (UTMP) [ 25 ], glucose transporter-1 [ 26 , 27 ], calbindin D9k [ 28 , 29 ], transient receptor potential channel type 6 [ 29 ], MMP-2 and 9 [ 21 ], SOLD1 [ 30 ], TIMP-2 [ 21 ], EMMPRIN, an inducer of MMPs [ 31 ], galectins 3, 4, and 9 [ 32 ], and COX-2 [ 33 , 34 ], SE is involved in numerous functions during different phases of pregnancy, such as histiotrophic nourishment of the fetus, materno-fetal glucose and calcium transfer, endometrial restructuring, immunomodulation in favor of the fetus, and oxytocin-induced prostaglandin F2alpha production at term. The expression of receptors for estrogens [ 15 , 35 ] growth hormone [ 36 ], various elements of the IGF system [ 37 ], prostaglandins E and F2alpha [ 33 , 34 ], oxytocin [ 38 ] and glucocorticoids [ 15 , 35 ], sheds a light on various hormones and other factors of maternal and fetal origin influencing SE function during pregnancy. The lack of progesterone receptors in the SE during pregnancy is overcome by progesterone-sensitive subepithelial stromal cells producing paracrine-acting factors, such as growth factors [ 37 ], which in turn regulate SE function via their receptors expressed on SE and thus may also initiate SE hypertrophy and hyperplasia.…”