Mel1c Mediated Monochromatic Light-Stimulated IGF-I Synthesis through the Intracellular Gαq/PKC/ERK Signaling Pathway
Mel1c Mediated Monochromatic Light-Stimulated IGF-I Synthesis through the Intracellular Gαq/PKC/ERK Signaling Pathway
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Mel1c 通过细胞内 G(α)q/PKC/ERK 信号通路介导单色光刺激 IGF-I 合成
DOI：
10.3390/ijms20071682
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发表时间：
2019-04-04
影响因子：
5.6
通讯作者：
Chen, Yaoxing
中科院分区：
文献类型：
--
作者：
Ning, Shujie;Wang, Zixu;Chen, Yaoxing
以前的研究表明，单色光影响血浆褪黑激素（MEL）水平，进而通过Mel 1c受体调节肝脏胰岛素样生长因子I（IGF-I）分泌。然而，由Mel 1c启动的细胞内信号通路仍不清楚。在这项研究中，新孵化的肉鸡，包括完整的，假手术，和松果体切除组，暴露于白色（WL），红色（RL），绿色（GL），或蓝色（BL）光14天。体内实验表明，GL显着促进血浆MEL形成，这是伴随着MEL受体，Mel 1c，以及磷酸化细胞外调节蛋白激酶（p-ERK 1/2），和IGF-I在肝脏中的表达增加，与其他光处理组相比。相反，这种GL刺激衰减松果体切除术。外源性MEL升高了肝细胞IGF-I水平，这与环磷酸腺苷（cAMP）、G（α）q、磷酸化蛋白激酶C（p-PKC）和p-ERK 1/2表达的增加一致。然而，Mel 1c选择性拮抗剂哌唑嗪抑制MEL诱导的IGF-I、G（α）q、p-PKC和p-ERK 1/2的表达，而cAMP浓度几乎不受影响。此外，用Ym 254890（G（alpha）q抑制剂）、Go 9863（PKC抑制剂）和PD 98059（ERK 1/2抑制剂）预处理显著减弱MEL刺激的IGF-I表达和p-ERK 1/2活性。这些结果表明，Mel 1c通过细胞内G（alpha）q/PKC/ERK信号转导介导单色GL刺激的IGF-I合成。
Previous studies have demonstrated that monochromatic light affects plasma melatonin (MEL) levels, which in turn regulates hepatic insulin-like growth factor I (IGF-I) secretion via the Mel1c receptor. However, the intracellular signaling pathway initiated by Mel1c remains unclear. In this study, newly hatched broilers, including intact, sham operation, and pinealectomy groups, were exposed to either white (WL), red (RL), green (GL), or blue (BL) light for 14 days. Experiments in vivo showed that GL significantly promoted plasma MEL formation, which was accompanied by an increase in the MEL receptor, Mel1c, as well as phosphorylated extracellular regulated protein kinases (p-ERK1/2), and IGF-I expression in the liver, compared to the other light-treated groups. In contrast, this GL stimulation was attenuated by pinealectomy. Exogenous MEL elevated the hepatocellular IGF-I level, which is consistent with increases in cyclic adenosine monophosphate (cAMP), G(alpha)q, phosphorylated protein kinase C (p-PKC), and p-ERK1/2 expression. However, the Mel1c selective antagonist prazosin suppressed the MEL-induced expression of IGF-I, G(alpha)q, p-PKC, and p-ERK1/2, while the cAMP concentration was barely affected. In addition, pretreatment with Ym254890 (a G(alpha)q inhibitor), Go9863 (a PKC inhibitor), and PD98059 (an ERK1/2 inhibitor) markedly attenuated MEL-stimulated IGF-I expression and p-ERK1/2 activity. These results indicate that Mel1c mediates monochromatic GL-stimulated IGF-I synthesis through intracellular G(alpha)q/PKC/ERK signaling.