Mechanism of prolactin action on induction of development, enlargement and inflammation of prostate -study with prolactin knockout mice-

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It is suggested that chronic hyperprolactinemia in infant mice induced by estrogen causes inflammation in the prostate. To prove the prolactin action on the prostate, extents of inflammation in wild-type and prolactin-knockout (PRL-KO) mice were examined after administration of an estrogenic compound, bisphenol A. The myeloperoxidase activity in the wild-type mice was increased by the treatment, but the activity remained at basal level in PRL-KO mice. These results indicate mat the inflammation ** the prostate is mediated by PRL. In order to clarify the molecular mechanisms of PRL action on the prostate, PRL-receptor (PRL-R) gene expression was analyzed. In addition of the known three first exons, El-1, El-2 and El-3, two novel first exons, El-4 and El-5, were identified in rat PRL-R gene. Each first exon is expressed in a tissue-specific manner. RT-PCR analysis repealed the expression of El-3 exon in the prostate. It has been known that the expression of El-3 was regulated by SP-1 and C/EBPβ, suggesting that the expression of PRL-R gene in the prostate is regulated by these two transcription factors.