ORIGINAL ARTICLE: Bcl‐2 and Bax Expressions in Pre‐Term, Term and Post‐Term Placentas
Problem Placental apoptosis-associated protein imbalance might contribute to the pathogenesis of pre- and post-term birth. Therefore, we evaluated the expression and distribution of pro-apoptotic (Bax) and anti-apoptotic (Bcl-2) molecules in term, pre-term and post-term placentas.
Method of study Placental samples were collected from women with term (n = 25), pre-term (n = 7) and post-term (n = 10) deliveries. The expression of Bcl-2 and Bax was assessed by immunochemistry on paraffin-embedded placental specimens.
Results The pattern of immunostaining for Bcl-2 and Bax was the same in all samples, but not the intensity. The Bax/Bcl-2 ratio was higher in both pre-term and post-term placental samples compared with term placentas as a result of intense reactivity for the pro-apoptotic factor, Bax in pre-term and post-term placentas and, for Bcl-2 decrease in pre-term placentas.
Conclusion These findings suggest that different unbalance mechanisms in placental apoptotic-associated protein expressions may be involved in the physiopathology of pre-term and post-term births.
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Available from: Yau-Huei Wei
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ABSTRACT: The endocrine disruptor 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) has been demonstrated to disrupt hormone signalling, reduce fertility, interfere with embryo development and cause spontaneous miscarriage in humans. The precise mechanisms of its effects on early implantation in humans are still unclear. In this study, we examined the relationship between mitochondrial function and dioxin-induced toxicity in JAR cells, a human trophoblast-like cell line. Several experiments were performed to address the effects of TCDD on cell viability, reactive oxygen species (ROS) generation, oxidative damage (indicated by the presence of lipoperoxides and oxidized DNA bases), mitochondrial DNA (mtDNA) copy number, ATP content, mtDNA mutations and the protein levels of p53, Bax, Bcl2, cytochrome c and caspase 3. Increased oxidative damage and mitochondrial dysfunction in TCDD-treated trophoblast-like cells was demonstrated. A 2.58-fold increase in lipid peroxides was detected in cells treated with 2 nM TCDD for 4 h. The oxidative DNA damage marker 8-hydroxy-2′-deoxyguanosine was significantly increased by TCDD treatment in a time-dependent manner. Meanwhile, reductions in mtDNA copy number and ATP content and an increase in mtDNA deletions were found. Furthermore, we observed increased apoptosis, p53 accumulation, Bax overexpression, cytochrome c release and sequential caspase 3 activation after TCDD exposure. These results indicate that oxidative damage and mitochondrial dysfunction may be responsible for the apoptotic effects of TCDD. © The Author 2010. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: [email protected]
Molecular Human Reproduction 05/2010; 16(5):361-72. DOI:10.1093/molehr/gaq004 · 3.75 Impact Factor
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ABSTRACT: With 2 figures and 2 tables
Apoptosis plays a central role in organ development, homeostasis and immune defence in multicellular organisms and is strictly controlled in part by members of Bcl-2 family. The Bcl-2 is a pro-survival molecule identified through its involvement in B-cell lymphomas. The aim of the study was to evaluate the incidence of apoptosis in the human placenta at different stages of pregnancy and to correlate it further with Bcl-2 expression. A total of 96 placental samples from first trimester, mid-trimester and uncomplicated term pregnancies were collected (n = 32 + 32 + 32). M30 cyto death monoclonal antibody was used to identify apoptotic cells. The apoptosis index of first trimester placentae was 2.33 ± 1.70, mid- trimester was 1.77 ± 1.36 and term placenta was 1.15 ± 0.21. Bcl-2 protein was found immunolocalized in the cytoplasm of syncytiotrophoblast. Apoptosis index was significantly reduced in term cases as compared with first trimester (P < 0.002) and mid-trimester placentae (P = 0.01). On the contrary, Bcl-2 expression was significantly higher at term cases than in first trimester (P < 0.0001) and mid-trimester cases (P < 0.001). The present study divulges the importance of apoptosis in permitting normal physiological turnover of villous trophoblast and also exhibits the contribution of bcl-2 in maintaining syncytial integrity throughout normal pregnancy.
Anantomia Histologia Embryologia 07/2010; 39(5):426-31. DOI:10.1111/j.1439-0264.2010.01012.x · 0.67 Impact Factor
Available from: Claire T Roberts
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ABSTRACT: The placenta is the intermediary between the mother and fetus, and its primary role is to provide for the appropriate growth of the fetus. A suboptimal in utero environment has been shown to differentially affect the health of offspring, depending on their sex. Here we show that excess maternal glucocorticoids administered in midgestation (Day 20, 0.5 gestation in the spiny mouse) for 60 h, have persisting effects on the placenta that differ by fetal sex, placental region, and time after glucocorticoid exposure. Dexamethasone (DEX) exposure altered placental structure and mRNA expression from male and female fetuses both immediately (Day 23) and 2 wk posttreatment (Day 37). The immediate consequences (Day 23) of DEX were similar between males and females, with reductions in the expression of IGF1, IGF1R, and SLC2A1 in the placenta. However, by Day 37, the transcriptional and structural response of the placenta was dependent on the sex of the fetus, with placentas of male fetuses having an increase in GCM1 expression, a decrease in SLC2A1 expression, and an increase in the amount of maternal blood sinusoids in the DEX-exposed placenta. Female placentas, on the other hand, showed increased SLC2A1 and MAP2K1 expression and a decrease in the amount of maternal blood sinusoids in response to DEX exposure. We have shown that the effect of a brief glucocorticoid exposure at midgestation has persisting effects on the placenta, and this is likely to have ongoing and dynamic effects on fetal development that differ for a male and female fetus.
Biology of Reproduction 07/2011; 85(5):1040-7. DOI:10.1095/biolreprod.111.093369 · 3.32 Impact Factor
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