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Figure 1 | Genome Medicine

Figure 1

From: The genomics of preterm birth: from animal models to human studies

Figure 1

Comparison of mouse and human parturition. (a) In mice, initial mechanisms for labor initiation include induction of uterine endometrial cyclooxygenase 1 (COX1) expression and reduction of uterine 15-hydroxyprostaglandin dehydrogenase (HPGD) expression. These changes in prostaglandin metabolism lead to elevated prostaglandin F (PGF), which acts on the ovarian corpus luteum to decrease circulating progesterone (P4). This systemic progesterone withdrawal results in induction of contraction-associated proteins (CAPs) and transition of the uterine myometrium from a quiescent to an actively contractile state. (b) In human pregnancy, labor initiation is associated with induction of amnion COX2 and placental corticotropin-releasing hormone (CRH) and a reduction in chorion HPGD. These changes in prostaglandin metabolism and peptide signaling are associated with increased amnion prostaglandin E2 (PGE2), pro-inflammatory cytokines and estradiol. This pro-inflammatory milieu is hypothesized to cause 'functional' progesterone withdrawal (circulating progesterone does not fall), or progesterone resistance, followed by induction of CAPs and labor. Note that several fundamental differences between human and mouse parturition exist beyond the differences in systemic progesterone regulation at term. Murine gestation is multi-fetal, whereas human gestation is predominantly single fetus. In mice, the sites of prostaglandin and progesterone synthesis are maternal, whereas in human pregnancy, the primary sites of prostaglandin and progesterone synthesis in late gestation are from fetal tissues. Adapted from [27], Ratajczak CK, Fay JC, Muglia LJ: Preventing preterm birth: the past limitations and new potential of animal models. Dis Model Mech 2010, 3: 407-14 with permission from The Company of Biologists.

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