Li Z, Shah G V
Department of Urologic Surgery, University of Kansas Medical Center, 66160, Kansas City, Kansas, USA.
Endocrine. 1995 Jun;3(6):453-9. doi: 10.1007/BF02935652.
Estrogens increase prolactin (PRL) synthesis and release in rats and humans, whereas pituitary-derived calcitonin-like immunoreactive peptide (pit-CT) inhibits PRL gene expression and release. To test the hypothesis that estrogens stimulate lactotrophs by diminishing pit-CT expression, the present studies examined effects of ovariectomy (ovx) and estradiol (E2) administration on (1) pit-CT IR cell population; (2) pit-CT IR content and (3) release of pit-CT IR by cultured anterior pituitary (AP) cells. Ability of anti-calcitonin immunoglobulins (anti-CT IgG) to stimulate PRL release from cultured AP cells was also examined. The results suggest that ovariectomy induced a large increase in pit-CT IR cell population in the AP gland and E2-treatment dramatically reversed this increase. Similar changes were observed in pit-CT IR content of AP extracts. Cultured AP cells from ovx rats released significantly higher amounts of pit-CT IR, and anti-CT IgG induced a significant increase in basal PRL release. AP cells from E2-treated rats secreted lower amounts of pit-CT IR and this was associated with significantly higher PRL release. These results suggest that estrogens may stimulate lactotrophs, at least in part, by removing inhibitory influence of endogenous pit-CT.
雌激素可增加大鼠和人类体内催乳素（PRL）的合成与释放，而垂体来源的降钙素样免疫反应性肽（pit-CT）则抑制PRL基因的表达和释放。为了验证雌激素通过减少pit-CT的表达来刺激催乳细胞这一假说，本研究检测了卵巢切除（ovx）和给予雌二醇（E2）对以下方面的影响：（1）pit-CT免疫反应细胞群体；（2）pit-CT免疫反应含量；（3）培养的垂体前叶（AP）细胞释放pit-CT免疫反应物质。还检测了抗降钙素免疫球蛋白（抗CT IgG）刺激培养的AP细胞释放PRL的能力。结果表明，卵巢切除导致AP腺中pit-CT免疫反应细胞群体大幅增加，而E2处理显著逆转了这一增加。AP提取物的pit-CT免疫反应含量也观察到类似变化。来自ovx大鼠的培养AP细胞释放的pit-CT免疫反应物质显著更多，抗CT IgG诱导基础PRL释放显著增加。来自E2处理大鼠的AP细胞分泌的pit-CT免疫反应物质较少，这与显著更高的PRL释放相关。这些结果表明，雌激素可能至少部分通过消除内源性pit-CT的抑制作用来刺激催乳细胞。
