Prostaglandin F2 alpha and E1 regulation of proliferation in primary cultures of rabbit endometrial cells.
Prostaglandin F2 alpha and E1 regulation of proliferation in primary cultures of rabbit endometrial cells.
复制标题
前列腺素 F2 α 和 E1 对兔子宫内膜细胞原代培养物增殖的调节。
DOI：
10.1002/jcp.1041270108
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发表时间：
1986
影响因子：
5.6
通讯作者：
Gerschenson,LE
中科院分区：
文献类型：
--
作者：
Orlicky,DJ;Lieberman,R;Gerschenson,LE
子宫内膜细胞生长的研究在生殖生物学中具有重要意义。一些因素和激素被认为在控制生长中起重要作用。前列腺素F2α（PGF 2 α）导致在无血清化学成分确定的培养基中培养的兔子宫内膜细胞的原代培养物的氚化胸苷（[3 H]Tdr）掺入DNA和细胞数量增加。与对照培养物相比，前列腺素F1α、E1、E2、A2和B2以及花生四烯酸（均在10− 7 M下检测）不影响[3 H]Tdr掺入。PGF 2 α刺激后DNA中[3 H]Tdr掺入量的增加具有浓度依赖性（最佳浓度为10 × 10− 7 M），并在刺激后109小时开始观察到。前列腺素E1（PGE 1）和前列腺素E2（PGE 2）均可拮抗并完全阻断PGF 2 α诱导的[3 H]Tdr掺入DNA的增加，但PGF 1 α、I2、A2、B2、其母体分子或相关分子均不能。当细胞在PGF 2 α刺激前用PGE 1预处理时，以及当细胞同时暴露于PGE 1和PGF 2 α时，均观察到这种拮抗作用。外源性添加8-Br-cAMP模拟PGE 1对PGF 2 α的拮抗作用。PGF 2 α诱导的[3 H]Tdr掺入增加与雌二醇-17 β或表皮生长因子引起的[3 H] Tdr掺入增加无协同、拮抗或相加作用。PGF 2 α对原代培养子宫内膜细胞生长的特异性作用以及PGE 1、PGE 2和8-Br-cAMP的拮抗作用是新发现。
The study of growth of endometrial cells is of importance in reproductive biology. Several factors and hormones are thought to play important roles in the control of growth. Prostaglandin F2α(PGF2α) causes an increase in both tritiated thymidine ([3H]Tdr) incorporation into DNA and in the cell number of primary cultures of rabbit endometrial cells cultured in a serum‐free, chemically defined media. Prostaglandins F1α, E1, E2, A2, and B2and arachidonic acid (all tested at 10−7M) do not affect [3H]Tdr incorporation as compared to control cultures. The increase in [3H]Tdr incorporation into DNA in response to PGF2αstimulation is concentration‐dependent (optimal ∼3 × 10−7M) and is seen starting ∼9 hr poststimulation. Both prostaglandin E1(PGE1) and prostaglandin E2(PGE2), but not PGs F1α, I2, A2, B2, their parent molecules, or related molecules, antagonize and can completely block the PGF2α‐induced increase in [3H]Tdr incorporation into DNA. This antagonism is seen both when the cells are pretreated with PGE1prior to the PGF2αstimulation and when the cells are exposed to both PGE1and PGF2αsimultaneously. Exogenously added 8‐Br‐cAMP mimics the PGE1antagonism of PGF2α. The PGF2α‐induced increase in [3H]Tdr incorporation is not synergistic, antagonistic, or additive with the [3H]Tdr incorporation increase in response to either estradiol‐17β or epidermal growth factor. The specific effect of PGF2αon primary culture endometrial cell growth and its antagonism by PGE1, PGE2, and 8‐Br‐cAMP are new findings.