Figure 7.

Increase in RARα at uterine implantation sites following pCR3.1-cyp26a1 immunization during mice peri-implantation and further certainty, the influence of RARα on Th17 cells at uterine implantation sites by tail vein injection of RARα specific agonist and antagonist during mice peri-implantation. (A) RARα levels were significantly increased at uterine implantation sites based on Western blotting. β-actin was used as a loading control. (B) RARα levels were obviously increased at implantation sites of D5 pregnancy based on immunohistochemistry following pCR3.1-cyp26a1 immunization; bars = 200 and 25 μm. The data were derived from three separate samples from pregnant mice. At least, three independent experiments were repeated for this time-point. A total of nine samples from pregnant mice were assessed. E, embryo; S, uterine stroma; LE, Luminal epithelium; GE, Glandular epithelium. (C) RARα and RORγt protein expression changes in uterus on D5 of pregnancy in response to administration of agonist (Am-580) and antagonist (Ro-41-5253) of RARα. RARα levels were significantly increased by the activation of Am-580 and significantly reduced by the inhibition of Ro-41-5253 at uterine implantation sites based on western blotting of pregnancy D5. RORγt levels just took the opposite changes on RARα. β-actin was used as a loading control. The administration (125 μg/mouse) of RARα agonist (Am-580) or antagonist (Ro-41-5253) was performed on D3 of pregnancy through tail vein injection; **P < 0.01. Three independent experiments were repeated for this time-point. The data were derived from three separate samples from pregnant mice. A total of nine samples from pregnant mice were assessed.