ECE2014 Poster Presentations Pituitary Basic (<emphasis role="italic">Generously supported by IPSEN</emphasis>) (11 abstracts)
Expression of peroxisome-proliferator activated receptor α in pituitary tumours
Sandra Rotondi 1 , Alessio Modarelli 1 , Lilya Rostomyan 2 , Maria Antonietta Oliva 3 , Vincenzo Esposito 3, , Luca Ventura 5 , Antonietta Arcella 3 , Edoardo Alesse 1 , Albert Beckers 2 & Marielise Jaffrain-Rea 1,
1Department of Biotechnological and Applied Clinical Sciences, University of L’Aquila, L’Aquila, Italy; 2Endocrinology, Centre Hospitalier
Universitaire de Liège, University of Liège, Liege, Belgium; 3Department of Neurological Sciences, Neuromed Institute, IRCCS, Pozzilli, Italy; 4Department of Neurology and Psychiatry, University of Rome “La Sapienza”, Rome, Italy; 5Pathology, San Salvatore Hospital, L’Aquila, Italy.
Peroxisome-proliferator activated receptors (PPARs) are involved in a number of neoplasia. PPARα (PPARα) is a partner of the aryl hydrocarbon receptor interacting protein (AIP), which is involved in the pathogenesis of pituitary adenomas (PA). We wished to investigate the potential expression and biological significance of PPARα in PA, especially in GH/PRL-secreting tumours.
Material and methods: A large series of PA was collected (n=110, 41 GH-, 14 PRL- and 55 non-functioning PA). PPARα expression was studied by semi-quantitative real-time PCR (qRT-PCR) in 84 PA and/or by semi-quantitative IHC in 74 PA, both of them being performed in 48 cases. PPARα IHC score was obtained by adding nuclear and cytoplasmic scores (range 0–6). Three normal post-mortem pituitaries (NP) were used as controls. The effect of fenofibrate on cell proliferation was studied in GH3 and MMQ cells.
Results: Data from qRT-PCR analysis suggested a down-regulation of PPARα mRNA in 28/84 PA (33.3%) as compared to NP. Overall, PPARα: βactin ratio were very low, with no significant difference between GH/PRL- and NFPA. However, significant PPARα immunoreactivity (score ≥ 2) was more frequently observed in GH/PRL- than in NFPA (82 vs 54.3%, P=0.009), resulting in a significantly higher score in GH/PRL-PA (P=0.0056 vs NFPA). The highest percentage of PPARα immunopositive nuclei was observed in PRLomas, followed by GH-secreting and NFPA (median 37, 25 and 18% respectively, P=0.08). No clear relationship could be observed between PPARα expression and tumour aggressiveness. In vitro treatment with fenofibrate (10–100 μM) induced a dose-dependent decrease in cell proliferation in GH3 cells but had no effect on MMQ cells, despite similar levels of PPARα protein were observed by western blot analysis.
Conclusion: PPARα is commonly expressed by PA, especially by GH/PRL-PA. The potential implications of such findings in terms of PA tumorigenesis and treatment should be further investigated.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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