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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,Mariam Alqaryyan,2 Majeda Al Zuabi,1 Nada Ayed,1 Modhi Khaled,1 Shaikhah Al Houli,1 Narayana Kilarkaje3

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Abstract

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.

Keywords

BAX, JNK, placenta, dexamethasone, intrauterine growth restriction

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