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The purpose of this study was to investigate a) PTTG expression in pituitary adenoma subtypes, b) the correlation between PTTG expression and clinico-pathological variables in patients with Cushing’s disease with ACTH secreting pituitary adenomas, and c) PTTG expression in brain tumour subtypes. PTTG expression was investigated in 89 pituitary and 88 brain tumours, and 54 ACTH adenomas of patients with Cushing’s disease. Our results show that PTTG is expressed in the cytoplasm of pituitary adenoma cells, and at higher levels in GH adenomas, with lower PTTG expression levels being exhibited by PRL adenomas. Significant differences were noted between PTTG expression in medically treated and non-treated GH adenomas. However, PTTG expression in ACTH adenomas did not correlate with clinico-pathological variables, making it an unsuitable prognostic indicator in such tumours. In brain neoplasms, PTTG was expressed at higher levels in malignant tumours, whereas in less aggressive tumours, PTTG expression was considerably lower.

The purpose of this study was to investigate a) PTTG expression in pituitary adenoma subtypes, b) the correlation between PTTG expression and clinico-pathological variables in patients with Cushing’s disease with ACTH secreting pituitary adenomas, and c) PTTG expression in brain tumour subtypes. PTTG expression was investigated in 89 pituitary and 88 brain tumours, and 54 ACTH adenomas of patients with Cushing’s disease. Our results show that PTTG is expressed in the cytoplasm of pituitary adenoma cells, and at higher levels in GH adenomas, with lower PTTG expression levels being exhibited by PRL adenomas. Significant differences were noted between PTTG expression in medically treated and non-treated GH adenomas. However, PTTG expression in ACTH adenomas did not correlate with clinico-pathological variables, making it an unsuitable prognostic indicator in such tumours. In brain neoplasms, PTTG was expressed at higher levels in malignant tumours, whereas in less aggressive tumours, PTTG expression was considerably lower.

Our previous study identified one candidate transcript, chicken prostaglandin D2 synthase (cPGDS), significantly higher expressed in hens with high-egg production across several chicken strains including the Single-Comb White Leghorn layers. To further elucidate its underlying molecular mechanisms, the downstream effects of cPGDS in primary culture of chicken anterior pituitary cells were investigated. We successfully generated a highly specific rabbit anti-cPGDS polyclonal antibody. Of 13 examined tissues/cells, quantitative reverse transcription polymerase chain reaction and Western blotting analysis demonstrated that cPGDS mRNA and protein were highly expressed in intestine, kidney, liver and pituitary gland. In addition, significantly higher cPGDS mRNA and protein expression levels of the pituitary gland and ovary in hens than of the pituitary gland and testis in roosters with the same age were found. Transfection of pEGFP-cPGDS plasmid into primary culture of pituitary anterior cells in medium that contained 1 mM arachidonic acids induced luteinizing hormone beta subunit (LHB) transcription and subsequent translation. Treatments of two metabolites in the cyclooxygenase pathway, PGD2 and PGJ2 in the primary culture of chicken anterior pituitary cells induced LHB transcription and translation in both dose- and time-dependent manners. Treatment of peroxisome proliferator activated receptors (PPARs) agonist increased LHB transcription and translation in chicken anterior pituitary cells. On the other hand, specific inhibitions of PPARA and PPARG using antagonists dramatically suppressed PGJ2-induced LHB transcription level. Taken together; these data suggested PGDS upregulated LHB transcription in primary culture of chicken anterior pituitary cells via the PPAR signaling pathway.

abstract / Biological Sciences / Doctoral / Doctor of Philosophy

No description available.