Are BAX and JNK involved in inhibition of placental growth in rats with dexamethasone-induced intrauterine growth restriction
- International Journal of Molecular Biology: Open Access
Amr Osman,1,2 Maie D Al Bader,2 Mariam Alqaryyan,2 Majeda Al Zuabi,1 Nada Ayed,1 Modhi Khaled,1 Shaikhah Al Houli,1 Narayana Kilarkaje3
PDF Full Text
Molecular mechanisms involved in the onset and progression of intrauterine growth restriction (IUGR) are not clear, although enhanced apoptosis seems to play a primary role. The present study investigated two key proteins, B-cell lymphoma associated X protein and c-Jun N-terminal kinase, in the basal and labyrinth zones of Dexamethasone-induced IUGR placenta. Pregnant Sprague-Dawley rats received daily intra-peritoneal injections of either dexamethasone or saline starting from 14 days of gestation to 21. Dams were sacrificed on day 19 and 21; fetuses and placentas were collected. IUGR was seen at day 21 with significantly reduced fetal weights (p<0.05). Gene and protein expressions of B-cell lymphoma associated X protein and c-Jun N-terminal kinase in the placental basal and labyrinth zones were investigated by real-time polymerase chain reaction, western blotting, and immune histochemistry. Expression of both B-cell lymphoma associated X protein and c-Jun N-terminal kinase mRNA decreased in the basal zone and increased in the labyrinth zone (p<0.05) with no significant change detected at the protein level. The increase in expression of both B-cell lymphoma associated X protein and c-Jun N-terminal kinase in the labyrinth zone may indicate that both signaling molecules have a significant role in the apoptosis of this zone.
BAX, JNK, placenta, dexamethasone, intrauterine growth restriction