Modulation of Bax expression in physiological and pathological human placentas throughout pregnancy.
Apoptosis is intimately involved in placental homeostasis, growth and remodelling, and apoptotic rates increase progressively during normal pregnancy as part of normal placental development. Moreover, apoptosis increases in pregnancies complicated by some pathologies such as preeclampsia, fetal growth restriction and diabetes. In the present study, we describe differences in the expression of proapoptotic protein Bax, in first trimester voluntary termination of pregnancy, first trimester abortion (reserved abortion), caesarean birth, spontaneous birth, preeclampsia and diabetes. We first observed a strong increase of Bax expression in the cytotrophoblast, stroma, endothelial cells and decidua of placentas of the first trimester abortion compared to the low/moderate Bax immunopositivity in all the placental compartments during the first trimester voluntary termination of pregnancy. Secondly, we showed a more intense immunopositivity for Bax in the third trimester spontaneous birth with respect to the third trimester caesarean birth. Thirdly, we observed an increase of Bax expression in preeclamptic placentas compared to the normal full-term placentas. In contrast, we observed a moderate Bax expression in diabetic placentas only slightly lower than the normal full-term placentas. Our results seem to suggest that deregulation of apoptotic turnover may lead to placental dysfunction and pathologies.
Cobellis
Luigi
L
Department of Gynecology, Obstetric and Reproductive Science Section of Clinical Anatomy, Second University of Naples, Italy.
De Falco
Maria
M
Torella
Marco
M
Trabucco
Elisabetta
E
Caprio
Francesca
F
Federico
Elisabetta
E
Manente
Lucrezia
L
Coppola
Gabriele
G
Laforgia
Vincenza
V
Cassandro
Roberto
R
Colacurci
Nicola
N
De Luca
Antonio
A
D002585:Cesarean Section; D016640:Diabetes, Gestational / Q000378:metabolism / Q000473:pathology; D005260:Female; D006262:Health; D006801:Humans; D010920:Placenta / Q000378:metabolism*; D011225:Pre-Eclampsia / Q000378:metabolism / Q000473:pathology; D011247:Pregnancy; D011261:Pregnancy Trimester, First / Q000378:metabolism; D011263:Pregnancy Trimester, Third / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000378:metabolism*
C494826:BAX protein, human; D051028:bcl-2-Associated X Protein