Glucocorticoid excess in utero inhibits fetal and placental growth and programs adverse health outcomes in adult offspring, including hypertension and metabolic disturbances. Maternal glucocorticoid access to placental and fetal tissues is regulated by metabolism through the 11beta-hydroxysteroid dehydrogenase (HSD11B) enzymes, as well as multidrug resistance P-glycoprotein (ABCB1)-mediated efflux of glucocorticoids from the placental syncytiotrophoblast layer.

The spiny mouse (Acomys cahirinus) has an extended gestation of 39 days and cortisol (not corticosterone) as its glucocorticoid, characteristics that make it a better model for human pregnancy than traditional rodent models. This study determined expression of mRNAs encoding the HSD11B isoforms (Hsd11b1 and Hsd11b2), the ABCB1 isoforms (Abcb1a and Abcb1b) and the glucocorticoid receptor (GR) in the junctional (JZ) and labyrinth zones (LZ) of the spiny mouse placenta across the second half of gestation (days 20, 25, 30, 34 and 37).

Expression of Hsd11b1 increased markedly from day 20 to 37 in both placental zones from male and female fetuses (all >30-fold, P<0.001), with LZ expression higher than JZ near term (P<0.001). LZ expression of Hsd11b2 was higher than in JZ (P<0.001) and peaked at day 25, after which it declined markedly towards term in both sexes. LZ expression of Abcb1a was higher than JZ expression for both sexes (P<0.001), and continued to rise throughout gestation to peak at term. Similarly, Abcb1b expression rose across gestation in both sexes (P<0.001), with gestational increases larger in the LZ than the JZ (P<0.001). Expression of GR was higher at term than mid-gestation in LZ tissue from both sexes (P<0.001), while only female JZ exhibited similar gestational increases.

Similar to other rodents, placental expression of Hsd11b2 in the spiny mouse peaks at mid-gestation but declines towards term. In contrast, increased LZ expression of the Abcb1 genes may limit placental glucocorticoid exposure in late gestation.