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首页> 外文期刊>Domestic Animal Endocrinology >Influence of brain plasmalogen changes on gonadotropin secretion from the cultured bovine anterior pituitary cells
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Influence of brain plasmalogen changes on gonadotropin secretion from the cultured bovine anterior pituitary cells

机译:脑血浆变化对培养牛前叶细胞的促性腺激素分泌的影响

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摘要

We recently discovered that the orphan G-protein–coupled receptor (GPR) 61 colocalized with GnRH receptors (GnRHRs) on the surface of most of bovine gonadotrophs. A recent study suggested that ethanolamine plasmalogen (PI) is a ligand for GPR61 in mouse neuroblastoma. Therefore, this study evaluated the hypothesis that PI alters LH and FSH secretion from cultured bovine anterior pituitary (AP) cells. We prepared bovine AP cells from postpubertal heifers (26?mo old) and cultured the cells for 3.5?d. We treated the cells with increasing concentrations (0, 5, 50, 500, 5,000, 50,000, or 500,000 pg/mL) of phosphoethanolamine PI (PEPI) extracted from the bovine brain, orl-α-lysophosphatidylethanolamine PI (LEPI) extracted from the bovine brain, for 5?min before either no treatment or GnRH stimulation. The medium samples were harvested 2?h after culture for LH and FSH assays. Phosphoethanolamine PI (50–500 pg/mL) stimulated (P 0.05) the basal secretion of FSH but not LH. Phosphoethanolamine PI at 50 pg/mL also enhanced (P 0.05) GnRH-induced FSH secretion. However, higher doses (500–500,000 pg/mL) of PEPI suppressed GnRH-induced FSH secretion. Moreover, 50 to 500,000 pg/mL PEPI suppressed GnRH-induced LH secretion. None of the tested concentrations of LEPI showed any effect on basal or GnRH-induced LH or FSH secretion. Pretreatment with Sma and Mad pathway inhibitors suppressed FSH secretion induced by PEPI, whereas an extracellular signal-regulated kinase pathway inhibitor blocked the PEPI-induced suppression of GnRH-stimulated LH secretion. Therefore, PEPI, but not LEPI, extracted from the bovine brain, alters FSH and LH secretion from cultured AP cells. Further studies are required to decide whether PEPI binds to GPR61 and whether PEPI plays an important role in the control of gonadotropin secretion from gonadotrophs.
机译:我们最近发现孤儿G蛋白偶联受体(GPR)61在大多数牛促性腺的表面上与GnRH受体(GNRHR)结合。最近的一项研究表明,乙醇胺浆(PI)是小鼠神经母细胞瘤的GPR61的配体。因此,该研究评估了PI改变LH和FSH分泌来自培养的牛前垂体(AP)细胞的假设。我们制备了从促产淘汰的小母牛(26?Mo旧)的牛AP细胞,并培养细胞3.5?d。从牛脑中提取的浓度(0,5,50,500,5,000,5,000,500,000,5,000,5,000,5,000,5,000pg / ml),从牛脑中提取的磷酸乙醇胺pi(ppi)的磷酸乙醇胺pi(ppi)的磷酸氯胺pi(ppi)的磷酸胺pi(lepi)的磷酸胺pi(ppi)的磷酸胺pi(lepi)的磷酸胺pi(ppi)的磷酸胺pi(ppi)的含量增加牛脑,在没有治疗或GnRH刺激之前为5?分钟。在培养后收获培养基样品2·h以获得LH和FSH测定。磷酸乙醇胺PI(50-500pg / ml)刺激(P <0.05)FSH的基础分泌,但不是LH。磷酸乙醇胺PI在50pg / ml中也增强(P <0.05)GNRH诱导的FSH分泌。然而,较高剂量(500-500,000pg / ml)的PpI抑制了GNRH诱导的FSH分泌。此外,50至500,000 pg / ml PpI抑制了GnRH诱导的LH分泌。没有一种测试的LEPI浓度显示出对基础或GNRH诱导的LH或FSH分泌的任何影响。用SMA和MAD途径抑制剂的预处理抑制了PEPI诱导的FSH分泌,而细胞外信号调节激酶途径抑制剂阻断了PEPI诱导的GNRH刺激的LH分泌的抑制。因此,从牛脑中提取的Pepi,但不是Lepi,改变了来自培养的AP细胞的FSH和LH分泌。需要进一步的研究来决定PEPI是否与GPR61结合,并且PEPI是否在从促性腺中控制促性腺激素分泌中发挥着重要作用。

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