The studies were based on the RAPD fingerprinting for the species identification of animals. The genomic DNA samples of ostriches, Taiwan local chickens, Aboracres broilers, Leghorn chickens, quails, doves, emus, Beltville small white turkeys, pheasants, Chinese geese, mule ducks, Holstein cattle and Landrace pigs were amplified with random primers by RAPD-PCR for fingerprinting. The results showed that the varied band patterns of DNA fingerprints were generated from templates depending on the kinds of primers or animal species. The same primer applied to the same breed, all of the main bands are similar, but which were different among species. In order to try to identify the species from the mixture of meat by RAPD fingerprinting, the meat of ostrich and cattle was mixed in different ratios for this study. The results showed that it could be easily and precisely distinguished according to the band distribution of RAPD patterns.
BackgroundProlactinoma is the most frequent pituitary tumor in humans. The dopamine D2 receptor agonist bromocriptine has been widely used clinically to treat human breast tumor and prolactinoma through inhibition of hyperprolactinemia and induction of tumor cell apoptosis, respectively, but the molecular mechanism of bromocriptine induction of pituitary tumor apoptosis remains unclear. Caveolin-1 is a membrane-anchored protein enriched on caveolae, inverted flask-shaped invaginations on plasma membranes where signal transduction molecules are concentrated. Currently, caveolin-1 is thought to be a negative regulator of cellular proliferation and an enhancer of apoptosis by blocking signal transduction between cell surface membrane receptors and intracellular signaling protein cascades. Rat pituitary adenoma GH3 cells, which express endogenous caveolin-1, exhibit increased apoptosis and shrinkage after exposure to bromocriptine. Hence, the GH3 cell line is an ideal model for studying the molecular action of bromocriptine on prolactinoma.ResultsThe expression of endogenous caveolin-1 in GH3 cells was elevated after bromocriptine treatment. Transiently expressed mouse recombinant caveolin-1 induced apoptosis in GH3 cells by enhancing the activity of caspase 8. Significantly, caveolin-1 induction of GH3 cell apoptosis was sensitized by the administration of bromocriptine. Phosphorylation of caveolin-1 at tyrosine 14 was enhanced after bromocriptine treatment, suggesting that bromocriptine-induced phosphorylation of caveolin-1 may contribute to sensitization of apoptosis in GH3 cells exposed to bromocriptine.ConclusionOur results reveal that caveolin-1 increases sensitivity for apoptosis induction in pituitary adenoma GH3 cells and may contribute to tumor shrinkage after clinical bromocriptine treatment.
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