Interleukin 6 inhibits mouse placental lactogen II but not mouse placental lactogen I secretion in vitro.
Interleukin 6 inhibits mouse placental lactogen II but not mouse placental lactogen I secretion in vitro.
复制标题
在体外，Interleukin 6 抑制小鼠胎盘催乳素 II 的分泌，但不抑制小鼠胎盘催乳素 I 的分泌。
DOI：
10.1073/pnas.90.24.11905
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发表时间：
1993
影响因子：
11.1
通讯作者：
Talamantes,F
中科院分区：
文献类型：
--
作者：
Yamaguchi,M;Ogren,L;Southard,JN;Kurachi,H;Miyake,A;Talamantes,F
小鼠胎盘产生几种属于催乳素-生长激素基因家族的多肽，包括小鼠胎盘催乳素（mPL）I和mPL-II。本研究旨在确定mPL-I和mPL-II的分泌是否受白细胞介素6（IL-6）的调节，IL-6存在于胎盘中，以前曾报道可刺激该基因家族垂体成员的分泌。人和小鼠IL-6对mPL-I和mPL-II分泌的影响在妊娠第7、9和12天的胎盘细胞的原代培养物中进行了检查。IL-6引起的剂量依赖性减少的mPL-II浓度在培养基中的细胞从第9和12天的怀孕，但不影响mPL-II浓度在培养基中的细胞从第7天的怀孕或mPL-I浓度在培养基中的细胞从第7天或第9天的怀孕。显著抑制mPL-II分泌的人IL-6的最低浓度为250 pM。IL-6对培养基中mPL-II浓度的影响主要是由于抑制mPL-II合成，这至少部分是由于mPL-II mRNA稳态水平的降低。这些数据提高了IL-6可能在体内调节中期妊娠后mPL-II产生的可能性。
The mouse placenta produces several polypeptides belonging to the prolactin-growth hormone gene family, including mouse placental lactogen (mPL) I and mPL-II. The present study was undertaken to determine whether the secretion of mPL-I and mPL-II is regulated by interleukin 6 (IL-6), which is present in the placenta and has previously been reported to stimulate the secretion of pituitary members of this gene family. Effects of human and mouse IL-6 on mPL-I and mPL-II secretion were examined in primary cultures of placental cells from days 7, 9, and 12 of pregnancy. IL-6 caused a dose-dependent reduction in the mPL-II concentration in the medium of cells from days 9 and 12 of pregnancy but did not affect the mPL-II concentration in the medium of cells from day 7 of pregnancy or the mPL-I concentration in the medium of cells from days 7 or 9 of pregnancy. The lowest concentration of human IL-6 that significantly inhibited mPL-II secretion was 250 pM. The effect of IL-6 on the mPL-II concentration in the medium was due primarily to inhibition of mPL-II synthesis, which resulted at least partly from a decrease in the steady-state level of mPL-II mRNA. These data raise the possibility that IL-6 may regulate mPL-II production after midpregnancy in vivo.