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首页> 外文期刊>The European Journal of Neuroscience >Insulin-like growth factor I (IGF-I) and its receptor (IGF-1R) in the rat anterior pituitary.
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Insulin-like growth factor I (IGF-I) and its receptor (IGF-1R) in the rat anterior pituitary.

机译：大鼠垂体前叶中的胰岛素样生长因子I（IGF-1）及其受体（IGF-1R）。

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摘要

Few and controversial results exist on the cellular sites of insulin-like growth factor (IGF)-I synthesis and the type 1 IGF receptor (IGF-1R) in mammalian anterior pituitary. Thus, the present study analysed IGF-I and the IGF-1R in rat pituitary. Reverse transcription-polymerase chain reaction revealed IGF-I and IGF-1R mRNA expression in pituitary. The sequences of both were identical to the corresponding sequences in other rat organs. In situ hybridization localized IGF-I mRNA in endocrine cells. The majority of the growth hormone (GH) cells and numerous adrenocorticotropic hormone (ACTH) cells exhibited IGF-1R-immunoreactivity at the cell membrane. At lower densities, IGF-1 receptors were also present at the other hormone-producing cell types, indicating a physiological impact of IGF-I for all endocrine cells. IGF-I-immunoreactivity was located constantly in almost all ACTH-immunoreactive cells. At the ultrastructural level, IGF-I-immunoreactivity was confined to secretory granules in co-existence with ACTH-immunoreactivity, indicating a concomitant release of both hormones. Occasionally, IGF-I-immunoreactivity was detected in an interindividually varying number of GH cells. In some individuals, weak IGF-I-immunoreactions were also detected also in follicle-stimulating hormone and luteinizing hormone cells. Thus, IGF-I seems to be produced as a constituent in ACTH cells, possibly indicating its particular importance in stress response. Generally, IGF-I from the endocrine cells may regulate synthesis and/or release of hormones in an autocrine/paracrine manner as well as prevent apoptosis and stimulate proliferation. Production of IGF-I in GH cells may depend on the physiological status, most likely the serum IGF-I level. IGF-I released from GH cells may suppress GH synthesis and/or release by an autocrine feedback mechanism in addition to the endocrine route.
机译：在哺乳动物垂体前叶中，胰岛素样生长因子（IGF）-I合成和1型IGF受体（IGF-1R）的细胞位点上几乎没有争议的结果。因此，本研究分析了大鼠垂体中的IGF-1和IGF-1R。逆转录聚合酶链反应显示垂体中的IGF-1和IGF-1R mRNA表达。两者的序列与其他大鼠器官中的相应序列相同。原位杂交将IGF-I mRNA定位在内分泌细胞中。大多数生长激素（GH）细胞和众多促肾上腺皮质激素（ACTH）细胞在细胞膜上均表现出IGF-1R免疫反应性。在较低的密度下，其他产生激素的细胞类型也存在IGF-1受体，表明IGF-1对所有内分泌细胞的生理影响。几乎所有ACTH免疫反应性细胞中均持续存在IGF-I免疫反应性。在超微结构水平上，IGF-I-免疫反应性与ACTH-免疫反应性共存仅限于分泌颗粒，表明两种激素同时释放。有时，在个体间变化的GH细胞中检测到IGF-I免疫反应性。在某些个体中，在促卵泡激素和促黄体生成素的荷尔蒙细胞中也检测到弱的IGF-I免疫反应。因此，IGF-I似乎作为ACTH细胞中的成分产生，可能表明其在应激反应中特别重要。通常，来自内分泌细胞的IGF-1可以以自分泌/旁分泌的方式调节激素的合成和/或释放，以及防止细胞凋亡和刺激增殖。 GH细胞中IGF-1的产生可能取决于生理状态，最可能取决于血清IGF-1的水平。从GH细胞释放的IGF-I除了内分泌途径外，还可以通过自分泌反馈机制抑制GH的合成和/或释放。

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