Brain injury and inflammation genes common to a number of neurological diseases and the genes involved in the genesis of GABAnergic neurons are altered in monoamine oxidase B knockout mice.
Brain injury and inflammation genes common to a number of neurological diseases and the genes involved in the genesis of GABAnergic neurons are altered in monoamine oxidase B knockout mice.
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DOI：
10.1016/j.brainres.2021.147724
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发表时间：
2022-01-01
期刊：
影响因子：
2.9
通讯作者：
Shih JC
中科院分区：
文献类型：
--
作者：
Chen K;Palagashvili T;Hsu W;Chen Y;Tabakoff B;Hong F;Shih AT;Shih JC
单胺氧化酶B（MAO B）氧化微量胺苯乙胺（PEA），以及大脑中的神经递质5-羟色胺和多巴胺。我们以前报道过，PEA水平在所有脑区显著增加，但血清素和多巴胺水平在MAO B敲除（KO）小鼠中没有变化。PEA和多巴胺都是由苯丙氨酸通过纹状体多巴胺能神经元中的芳香族L-氨基酸脱羧酶合成的。纹状体中高浓度的PEA可在不存在MAO B的情况下引起多巴胺能神经元死亡。我们从MAO B KO小鼠（2月龄）和年龄匹配的野生型（WT）雄性小鼠的脑组织中分离RNA，并通过Affyssin微阵列分析改变的基因。通过Partek Genomics Suite分析了与WT小鼠相比，MAO B KO中的差异表达基因（DEG），然后进行了免疫途径分析（IPA），以评估其功能关系。MAO B KO小鼠中的DEG参与脑炎症和GABA能神经元的发生。显著的DEG包括四种脑损伤或炎症基因（上调：Ido 1、TSPO、AVP、Tdo 2），五种γ-氨基丁酸（GABA）受体（下调：GABRA 2、GABRA 3、GABRB 1、GABRB 3、GABRG 3），五种与成人神经发生相关的转录因子（上调：Wnt 7b、Hes 5;下调：Pax 6、Tcf 4、Dtna）。在MAO B敲除小鼠中改变的脑损伤和炎症基因涉及各种神经障碍：注意缺陷多动障碍、惊恐障碍、强迫症、自闭症、肌萎缩性侧索硬化症、帕金森病、阿尔茨海默病、双相情感障碍。许多人通常参与这些疾病，表明有重叠的分子途径。
Monoamine oxidase B (MAO B) oxidizes trace amine phenylethylamine (PEA), and neurotransmitters serotonin and dopamine in the brain. We reported previously that PEA levels increased significantly in all brain regions, but serotonin and dopamine levels were unchanged in MAO B knockout (KO) mice. PEA and dopamine are both synthesized from phenylalanine by aromatic L-amino acid decarboxylase in dopaminergic neurons in the striatum. A high concentration of PEA in the striatum may cause dopaminergic neuronal death in the absence of MAO B. We isolated the RNA from brain tissue of MAO B KO mice (2-month old) and age-matched wild type (WT) male mice and analyzed the altered genes by Affymetrix microarray. Differentially expressed genes (DEGs) in MAO B KO compared to WT mice were analyzed by Partek Genomics Suite, followed by Ingenuity Pathway Analysis (IPA) to assess their functional relationships. DEGs in MAO B KO mice are involved in brain inflammation and the genesis of GABAnergic neurons. The significant DEGs include four brain injury or inflammation genes (upregulated: Ido1, TSPO, AVP, Tdo2), five gamma-aminobutyric acid (GABA) receptors (down-regulated: GABRA2, GABRA3, GABRB1, GABRB3, GABRG3), five transcription factors related to adult neurogenesis (upregulated: Wnt7b, Hes5; down-regulated: Pax6, Tcf4, Dtna). Altered brain injury and inflammation genes in MAO B knockout mice are involved in various neurological disorders: attention deficit hyperactive disorder, panic disorder, obsessive compulsive disorder, autism, amyotrophic lateral sclerosis, Parkinson’s diseases, Alzheimer’s disease, bipolar affective disorder. Many were commonly involved in these disorders, indicating that there are overlapping molecular pathways.
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DOI：
10.1016/j.bbamcr.2010.09.010
发表时间：
2011-07
期刊：
Biochimica et biophysica acta
影响因子：
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