ECE2016 Eposter Presentations Pituitary - Basic (17 abstracts)
Polychlorinated biphenyls affect apoptosis of pituitary cells through extrinsic and intrinsic pathways
Francesco Raggi 1 , Dania Russo 1 , Claudio Urbani 1, , Daniele Cappellani 1 , Luca Manetti 1 , Chiara Sardella 1 , Isabella Lupi 1 , Ilaria Scattina 1 , Luca Tomisti 1 , Claudio Marcocci 1 , Enio Martino 1 & Fausto Bogazzi 1
1University of Pisa, Pisa, Italy; 2Sant’Anna School of Advanced Study, Pisa, Italy.
Introduction: Polychlorinated biphenyls (PCBs) are environmental pollutants that modulate endocrine functions, induce tumorigenesis, and regulate apoptosis in several tissues; however, their effects on the apoptosis of pituitary cells is unknown.
The aim of this study was to evaluate the PCBs influence on the apoptosis of normal pituitary cells and elucidate the molecular mechanisms involved.
Methods: Primary cell cultures from mouse pituitary glands were exposed to a PCBs mixture (Aroclor 1254) or dioxin-like (PCB-77, PCB-126) or non-dioxin-like (PCB-153, PCB-180) congeners. Apoptosis was assessed by Annexin V staining, DNA fragmentation, and TUNEL assay. The expression and activity of intrinsic and extrinsic pathways were evaluated by Western blot. Thyroid hormone receptor (TR), aryl-hydrocarbon receptor (AhR), and CYP1A1 antagonists were used to examine the mechanisms of PCBs action.
Results: Aroclor 1254 induced apoptosis of pituitary cells as well as an increase in the expression and activity of caspase-8 and caspase-3, whereas the expression and activity of caspase-9 was unmodified. PCB-180 affected the extrinsic pathways by an increase in the expression of TNF-α, TRAIL and TRADD whereas PCB-153 reduced the apoptosis through a decrease in the expression of TNF-α, FAS-L, TRADD, and FADD. The intrinsic pathway was not influenced by PCB-180 whereas PCB-153 affected it by an increase of PI3K-AKT and a reduction of the p38–p53 pathways. The anti-apoptotic phenotype of PCB-153 was counteracted by a TR or CYP1A1 antagonists, whereas the pro-apoptotic effect of PCB 180 was prevented by an AhR antagonist. In contrast, the dioxin-like congeners did not affect apoptosis. The apoptosis induced by Aroclor 1254 or PCB-180 was associated with a reduction in cell proliferation, whereas the decreased apoptosis due to PCB-153 increased cell proliferation by 30%.
Conclusions: Non-dioxin-like PCBs may modulate apoptosis and the proliferation rate of pituitary cells having pro- or anti-apoptotic effects depending on specific congeners.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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