Stimulation of prostaglandin E2 synthesis in cloned osteoblastic cells of mouse (MC3T3-E1) by epidermal growth factor.
Stimulation of prostaglandin E2 synthesis in cloned osteoblastic cells of mouse (MC3T3-E1) by epidermal growth factor.
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表皮生长因子刺激小鼠克隆成骨细胞 (MC3T3-E1) 中前列腺素 E2 的合成。
DOI：
10.1016/s0021-9258(18)66726-2
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
M. Kumegawa
中科院分区：
文献类型：
--
作者：
K. Yokota;M. Kusaka;T. Ohshima;S. Yamamoto;N. Kurihara;T. Yoshino;M. Kumegawa
前列腺素 (PG) E2 被称为骨吸收因子，在从小鼠颅骨克隆的成骨细胞系 (MC3T3-E1) 的培养基中作为主要的花生四烯酸代谢物释放。表皮生长因子 (EGF) (10 ng/ml) 显着增强内源性 PGE2 合成，需要牛血清中同时存在未识别的因子。 PGE2 合成在 1-2 小时的滞后期后增加，并在添加 EGF 后约 3 小时达到最高水平。 EGF刺激的PGE2合成几乎被10μM放线菌酮或1μM放线菌素D完全阻断。此外，当用EGF预处理细胞时，微粒体表现出脂肪酸环氧合酶（花生四烯酸----PGH2）的活性增加，而PGE合酶（PGH2----PGE2）的活性保持不变。这些结果表明 EGF 介导的环氧合酶诱导。 PGE2 合成增加后，DNA 合成增加，碱性磷酸酶活性降低，对 EGF 的反应减慢。添加到细胞中的 PGE2（高于 0.1 µM）可以替代 EGF。然而，EGF对成骨细胞的这种作用不能完全归因于EGF刺激产生的PGE 2 的自分泌功能，因为EGF的这些作用不能被吲哚美辛消除，吲哚美辛阻断PGE 2 的合成。
Prostaglandin (PG) E2, known as a bone-resorption factor, was released as a predominant arachidonate metabolite in the culture medium of an osteoblastic cell line cloned from mouse calvaria (MC3T3-E1). Epidermal growth factor (EGF) (10 ng/ml) prominently enhanced endogenous PGE2 synthesis, requiring the simultaneous presence of unidentified factor(s) contained in bovine serum. PGE2 synthesis increased after a lag phase for 1-2 h and reached a maximum level at about 3 h after EGF addition. EGF-stimulated PGE2 synthesis was almost completely blocked by 10 microM cycloheximide or 1 microM actinomycin D. Furthermore, when the cells were pretreated with EGF, the microsomes exhibited an increased activity of fatty acid cyclooxygenase (arachidonic acid----PGH2), whereas the activity of PGE synthase (PGH2----PGE2) remained unchanged. These results suggested an EGF-mediated induction of cyclooxygenase. Following increased PGE2 synthesis, DNA synthesis increased and alkaline phosphatase activity decreased in a slower response to EGF. PGE2 (above 0.1 microM) added to the cells could replace EGF. However, such effects of EGF on the osteoblasts could not be attributed totally to an autocrine function of PGE2 produced by stimulation with EGF because these effects of EGF were not abolished by indomethacin, which blocked the PGE2 synthesis.