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

提示雌性激素引起的幼鼠慢性高泌乳素血症可引起前列腺炎症。为了证明催乳素对前列腺的作用，在给药一种雌激素化合物双酚a后，研究了野生型和催乳素敲除（PRL-KO）小鼠的炎症程度。野生型小鼠的髓过氧化物酶活性增加，但PRL-KO小鼠的活性保持在基础水平。提示前列腺炎症**是由PRL介导的。为了阐明PRL作用于前列腺的分子机制，我们对PRL受体（PRL- r）基因表达进行了分析。除了已知的三个前外显子El-1、El-2和El-3外，还在大鼠PRL-R基因中发现了两个新的前外显子El-4和El-5。每个第一个外显子以组织特异性的方式表达。RT-PCR分析证实El-3外显子在前列腺中的表达。已知El-3的表达受SP-1和C/EBPβ的调控，提示前列腺PRL-R基因的表达受这两种转录因子的调控。

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 RT-PCR analysis repealed the expression of El-3 exon in the prostate.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.