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白细胞介素-1β和前列腺素E2在PC12细胞中诱导芳香族L-氨基酸脱羧酶信使核糖核酸的表达。

Induction of aromatic L-amino acid decarboxylase mRNA by interleukin-1 beta and prostaglandin E2 in PC12 cells.

作者信息

Li X M, Juorio A V, Boulton A A

机构信息

Neuropsychiatry Units, University of Saskatchewan, Saskatoon, Canada.

出版信息

Neurochem Res. 1994 May;19(5):591-5. doi: 10.1007/BF00971335.

DOI:10.1007/BF00971335
PMID:8065515
Abstract

Aromatic 1-amino acid decarboxylase (AADC) is involved in the synthesis of the putative neurotransmitters dopamine (DA), norepinephrine (NA) and 5-hydroxytryptamine (5-HT). We report here that the gene expression of AADC can be regulated by interleukin (IL) 1-beta and prostaglandin (PG) E2 in PC12 cells. The cells were treated with different doses of IL 1-beta and PGE2 for 3 days. Slot blot hybridization was performed to detect AADC mRNA and Western immunoblot to detect AADC protein. The cDNA probe for rat AADC was generated by the PCR method. IL 1-beta and PGE2 produced a dose- and time-dependent up-regulation in AADC mRNA levels (up to 200% of the control values) which was followed by a stable increase in AADC protein. The data further support the suggestion that AADC is a regulated enzyme and that the regulation occurs at the level of gene expression. Because IL-1 is synthesized, and acts locally, within the brain to influence neuronal and glial functions, it has been proposed to be a mediator with both beneficial and detrimental responses to inflammation and injury. The regulation of AADC by IL-1 may indicate a possible involvement for AADC in neuronal injury and recovery. Since IL-1 promotes PGE2 formation, its effects may be occurring by increasing level of PGE2.

摘要

芳香族1-氨基酸脱羧酶(AADC)参与了假定神经递质多巴胺(DA)、去甲肾上腺素(NA)和5-羟色胺(5-HT)的合成。我们在此报告,在PC12细胞中,AADC的基因表达可受白细胞介素(IL)-1β和前列腺素(PG)E2的调控。用不同剂量的IL-1β和PGE2处理细胞3天。进行狭缝印迹杂交以检测AADC mRNA,进行蛋白质免疫印迹以检测AADC蛋白。大鼠AADC的cDNA探针通过PCR方法制备。IL-1β和PGE2使AADC mRNA水平呈剂量和时间依赖性上调(高达对照值的200%),随后AADC蛋白稳定增加。这些数据进一步支持了AADC是一种受调控的酶且调控发生在基因表达水平的观点。由于IL-1在脑内合成并在局部发挥作用以影响神经元和神经胶质细胞功能,因此有人提出它是一种对炎症和损伤具有有益和有害反应的介质。IL-1对AADC的调控可能表明AADC可能参与神经元损伤和恢复。由于IL-1促进PGE2的形成,其作用可能是通过提高PGE2水平而发生的。

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