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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Signal transduction pathways and tyrosine hydroxylase regulation in the adrenal medulla following glucoprivation: an in vivo analysis.
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Signal transduction pathways and tyrosine hydroxylase regulation in the adrenal medulla following glucoprivation: an in vivo analysis.

机译：糖缺乏后肾上腺髓质中的信号转导途径和酪氨酸羟化酶调节：体内分析。

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摘要

The regulation of tyrosine hydroxylase (TH, the rate limiting enzyme involved in catecholamine synthesis) is critical for the acute and sustained release of catecholamines from adrenal medullary chromaffin cells, however the mechanisms involved have only ever been investigated under in vitro/in situ conditions. Here we explored the effects on, TH phosphorylation and synthesis, and upstream signalling pathways, in the adrenal medulla evoked by the glucoprivic stimulus, 2-deoxy-d-glucose (2DG) administered intraperitoneally to conscious rats. Our results show that 2DG evoked expected increases in plasma adrenaline and glucose at 20 and 60min. We demonstrated that protein kinase A (PKA) and cyclin dependent kinases (CDK) were activated 20min following 2DG, whereas mitogen activated protein kinase (MAPK) was activated later and PKC was not significantly activated. We demonstrated that phosphorylation of Ser40TH peaked after 20min whereas phosphorylation of Ser31TH was still increasing at 60min. Serine 19 was not phosphorylated in this time frame. TH phosphorylation also occurred on newly synthesized protein 24h after 2DG. Thus 2DG increases secretion of adrenaline into the plasma and the consequent rise in glucose levels. In the adrenal medulla 2DG activates PKA, CDK and MAPK, and evokes phosphorylation of Ser40 and Ser31 in the short term and induces TH synthesis in the longer term all of which most likely contribute to increased capacity for the synthesis of adrenaline.
机译：酪氨酸羟化酶（TH，参与儿茶酚胺合成的限速酶）的调节对于从肾上腺髓质嗜铬细胞中急性和持续释放儿茶酚胺至关重要，但是所涉及的机制仅在体外/原位条件下进行过研究。在这里，我们探讨了通过糖皮质激素刺激，腹膜内给予有意识大鼠的2-脱氧-d-葡萄糖（2DG）引起的肾上腺髓质中对TH磷酸化和合成以及上游信号通路的影响。我们的结果表明2DG在20和60分钟时诱发了血浆肾上腺素和葡萄糖的预期增加。我们证明了蛋白激酶A（PKA）和细胞周期蛋白依赖性激酶（CDK）在2DG后20分钟被激活，而有丝分裂原激活的蛋白激酶（MAPK）随后被激活，而PKC没有被显着激活。我们证明，Ser40TH的磷酸化在20分钟后达到峰值，而Ser31TH的磷酸化在60分钟时仍在增加。在此时间范围内，丝氨酸19未被磷酸化。 2DG后24h，TH的磷酸化也发生在新合成的蛋白质上。因此2DG增加了肾上腺素向血浆中的分泌，并因此增加了葡萄糖水平。在肾上腺髓质中，2DG可在短期内激活PKA，CDK和MAPK，并引起Ser40和Ser31的磷酸化，并在长期内诱导TH合成，所有这些极有可能有助于增加肾上腺素的合成能力。

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