Differential actions of arachidonic acid and melittin on luteinizing hormone release and synthesis.
Differential actions of arachidonic acid and melittin on luteinizing hormone release and synthesis.
复制标题
花生四烯酸和蜂毒肽对黄体生成素释放和合成的不同作用。
DOI：
10.1159/000125178
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发表时间：
1989
影响因子：
4.1
通讯作者：
Jackson,GL
中科院分区：
文献类型：
--
作者：
Liu,TC;Jackson,GL
我们通过培养的大鼠垂体前叶细胞研究了花生四烯酸 (AA) 对黄体生成素 (LH) 释放与合成（翻译或糖基化）的作用。将单层细胞与促分泌素（AA、蜂毒肽、促性腺激素释放激素；GnRH）一起孵育 3-4 小时，从而增加内源性 AA 水平或释放 AA。通过分别测量[14C]丙氨酸和[3H]葡萄糖胺掺入总（细胞加培养基）免疫沉淀LH中来监测LH翻译和糖基化。通过放射免疫测定法测量免疫反应性 (IR) LH。 AA 的非裂解剂量增加 (p < 0.01) IR-LH 释放，但不增加总 [3H] 葡萄糖胺-LH、[14C]丙氨酸-LH 或 [3H]葡萄糖胺-蛋白。 AA要么没有影响，要么略微增加(p < 0.05) [ 3 H]葡萄糖胺摄取，但减少( p < 0.01) [ 14 C]丙氨酸摄取和总[ 14 C]丙氨酸蛋白的掺入。 250 µM 裂解细胞的 AA，从而增加培养基 IR-LH 并减少（p < 0.01 [3H]葡萄糖胺和 [l4C]丙氨酸摄取和掺入总 LH 和蛋白质。蜂毒肽通过激活磷脂酶 A2（245 和 490 nM）释放 AA，增加培养基 IR-LH (p < 0.0l)，而不影响测量的任何其他参数。 GnRH 在 1 n 时增强 (p < 0.01) LH（IR-LH、[3H]葡萄糖胺-LH 和 [14C]丙氨酸-LH）释放和总 [3H]葡萄糖胺-LH，但对总 [14C]丙氨酸-LH 没有影响。 总之，刺激 LH 释放的 AA 和蜂毒肽不会刺激 LH 糖基化或翻译。非特异性促分泌素增加的 LH 释放不一定伴随着 LH 糖基化或翻译的增加。
We studied the actions of arachidonic acid (AA) on luteinizing hormone (LH) release versus synthesis (translation or glycosylation) by cultured rat anterior pituitary cells. Monolayer cells were incubated for 3–4 h with secretagogues (AA, melittin, gonadotropin-releasing hormone; GnRH) which either increase endogenous AA levels or release AA. LH translation and glycosylation were monitored by measuring the incorporation of [14C]alanine and [3H]glucosamine, respectively, into total (cell plus medium) immunoprecipitable LH. Immunoreactive (IR) LH was measured by radioimmunoassay. Nonlytic doses of AA increased (p < 0.01) IR-LH release without increasing total [3H]glucosamine-LH, [14C]alanine-LH, or [3H]gIucosamine-protein. AA either had no effect or slightly increased (p < 0.05) [3H]glucosamine uptake, but decreased (p < 0.01) [14C]alanine uptake and incorporation into total [l4C]alanine protein. AA at 250 µMlysed cells, thus increasing medium IR-LH and decreasing (p < 0.01 [3H]glucosamine and [l4C]alanine uptake and incorporation into total LH and protein. Melittin, which releases AA by activating phospholipase A2 (245 and 490 nM), increased medium IR-LH (p . < 0.0l) without affecting any other parameter measured. GnRH at 1 nMenhanced (p < 0.01) both LH (IR-LH, [3H]glucosamine-LH and [14C]alanine-LH) release and total [3H]glucosamine-LH, but had no effect on total [14C]alanine-LH. In summary, AA and melittin at doses which stimulated LH release did not stimulate either LH glycosylation or translation. This suggests that increased LH release by nonspecific secretagogues is not necessarily accompanied by increased LH glycosylation or translation.