Immunocytochemical localization of monoamine oxidases A and B in human peripheral tissues and brain.

Thorpe, L. W.; Westlund, Karin N.; Kochersperger, Lynn; Abell, Creed W.; Denney, Richard M.

doi:10.1177/35.1.3025289

Cited by 155 publications

(82 citation statements)

References 28 publications

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“…45 As does the MAOA enzyme, MAOB also degrades monoamines, but with a different substrate preference: MAOB has higher affinity for DA, 46,47 phenylethylamine 48,49 and benzylamine, 50 whereas MAOA displays higher affinity for NA and 5-HT. Further, both enzymes are expressed in the central nervous system (CNS) but with different distributions: MAOB is preferentially expressed on serotonergic 51 and histaminergic 52 neurons, while MAOA is mainly expressed in noradrenergic neurons. 51,53 Both genes are expressed in glia.…”

Section: Discussionmentioning

confidence: 99%

“…Further, both enzymes are expressed in the central nervous system (CNS) but with different distributions: MAOB is preferentially expressed on serotonergic 51 and histaminergic 52 neurons, while MAOA is mainly expressed in noradrenergic neurons. 51,53 Both genes are expressed in glia. 52 Since MAOB is a regulator of monoamine tone and is expressed in the brain, it is a logical candidate for susceptibility to neuropsychiatric diseases.…”

Section: Discussionmentioning

confidence: 99%

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Interaction between a functional MAOA locus and childhood sexual abuse predicts alcoholism and antisocial personality disorder in adult women

et al. 2007

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Women who have experienced childhood sexual abuse (CSA) have an increased risk of alcoholism and antisocial personality disorder (ASPD). Among male subjects, a functional polymorphism (MAOA-LPR, monoamine oxidase A linked polymorphic region) in the promoter region of the monoamine oxidase A gene (MAOA) appears to moderate the effect of childhood maltreatment on antisocial behavior. Our aim was to test whether MAOA-LPR influences the impact of CSA on alcoholism and ASPD in a sample of 291 women, 50% of whom have experienced CSA; we also tested whether haplotypes covering the region where both MAOA and monoamine oxidase B (MAOB) genes are located predict risk of alcoholism and ASPD better than the MAOA-LPR locus alone. Participants included 168 alcoholics (39 with ASPD (antisocial alcoholics) and 123 controls (no alcoholics, no ASPD). Antisocial behavior was also modeled as a continuous trait: ASPD symptoms count. The MAOA-LPR low activity allele was associated with alcoholism (P = 0.005), particularly antisocial alcoholism (P = 0.00009), only among sexually abused subjects. Sexually abused women who were homozygous for the low activity allele had higher rates of alcoholism and ASPD, and more ASPD symptoms, than abused women homozygous for the high activity allele. Heterozygous women displayed an intermediate risk pattern. In contrast, there was no relationship between alcoholism/antisocial behavior and MAOA-LPR genotype among non-abused women. The MAOA-LPR low activity allele was found on three different haplotypes. The most abundant MAOA haplotype containing the MAOA-LPR low activity allele was found in excess among alcoholics (P = 0.008) and antisocial alcoholics (P = 0.001). Finally, a MAOB haplotype, which we termed haplotype C, was significantly associated with alcoholism (P = 0.006), and to a lesser extent with antisocial alcoholism (P = 0.03). In conclusions, MAOA seems to moderate the impact of childhood trauma on adult psychopathology in female subjects in the same way as previously shown among male subjects. The MAOA-LPR low activity allele appears to confer increased vulnerability to the adverse psychosocial consequences of CSA. Haplotype-based analysis of the MAOA gene appeared to strengthen the association, as compared to the MAOA-LPR locus alone. A MAOB haplotype was associated with alcoholism independently from ASPD.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Interaction between a functional MAOA locus and childhood sexual abuse predicts alcoholism and antisocial personality disorder in adult women

et al. 2007

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“…Placenta and fibroblasts predominantly express MAO A (4,5), and platelets and lymphocytes express only MAO B (6). In the brain, even though MAO A prefers 5-hydroxytryptamine and MAO B prefers PEA as substrate, MAO B but not MAO A was found in serotonergic neurons (7,8). MAO A was expressed in catecholaminergic neurons, whereas MAO B is rich in astrocytes.…”

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confidence: 99%

Dual Functions of Transcription Factors, Transforming Growth Factor-β-inducible Early Gene (TIEG)2 and Sp3, Are Mediated by CACCC Element and Sp1 Sites of Human Monoamine Oxidase (MAO) B Gene

Chen

Shih

2004

Journal of Biological Chemistry

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Monoamine oxidases (MAO)A and B catalyze the oxidative deamination of many biogenic and dietary amines. Abnormal expression of MAO has been implicated in several psychiatric and neurodegenerative disorders. Human MAO B core promoter (؊246 to ؊99 region) consists of CACCC element flanked by two clusters of overlapping Sp1 sites. Here, we show that cotransfection with transforming growth factor (TGF)-␤-inducible early gene (TIEG)2 increased MAO B gene expression at promoter, mRNA, protein, and catalytic activity levels in both SH-SY5Y and HepG2 cells. Mutation of the CACCC element increased the MAO B promoter activity, and cotransfection with TIEG2 further increased the promoter activity, suggesting that CACCC was a repressor element. This increase was reduced when the proximal Sp1 overlapping sites was mutated. Similar interactions were found with Sp3. These results showed that TIEG2 and Sp3 were repressors at the CACCC element but were activators at proximal Sp1 overlapping sites of MAO B. Gel-shift and chromatin immunoprecipitation assays showed that TIEG2 and Sp3 bound directly to CACCC element and the proximal Sp1 sites in both synthetic oligonucleotides and natural MAO B core promoter. TIEG2 had a higher affinity to Sp1 sites than CACCC element, whereas Sp3 had an equal affinity to both elements. Thus, TIEG2 was an activator, but Sp3 had no effect on MAO B gene expression. This study provides new insights into MAO B gene expression and illustrates the complexity of gene regulation.Monoamine oxidase (MAO) 1 plays an important role in the metabolism of biogenic amines, including serotonin (5-hydroxytryptamine), norepinephrine, dopamine, tyramine, and phenylethylamine (PEA). There are two isoenzymes of MAO (MAO A and MAO B) that exhibit distinct substrate and inhibitor specificity (1, 2; for review, see Ref.3). Although both forms of MAO are expressed throughout the body, they differ in celland tissue-specific expressions. Placenta and fibroblasts predominantly express MAO A (4, 5), and platelets and lymphocytes express only MAO B (6). In the brain, even though MAO A prefers 5-hydroxytryptamine and MAO B prefers PEA as substrate, MAO B but not MAO A was found in serotonergic neurons (7,8). MAO A was expressed in catecholaminergic neurons, whereas MAO B is rich in astrocytes. Moreover, MAO B but not MAO A activity increases progressively in the brain throughout adult life (7, 9).MAO A and MAO B are coded by different genes (10) and are closely linked on X chromosome, Xp11.2-11.4 (11). Both consist of 15 exons with identical exon-intron organization (12). The promoter of MAO A has bi-directional activity (13) and consists of a functional polymorphism in a 30-bp repeat sequence (14). The 5Ј-flanking sequence of MAO B gene has been characterized. The maximal promoter activity for MAO B gene was found to be in the Ϫ246 to Ϫ99 region. This region consists of two clusters of overlapping Sp1 sites separated by a CACCC element (15). Previously, we have shown that Sp1 and Sp3 can bind to both proximal and distal clusters...

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“…Monoamine oxidases (MAO) are catalytic enzymes prevalent in the brain and peripheral tissue (6). Present as two structurally distinct isoforms, MAO A and MAO B both degrade monoamine neurotransmitters and produce hydrogen peroxide as a toxic byproduct (7).…”

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confidence: 99%

Mechanistic Role for a Novel Glucocorticoid-KLF11 (TIEG2) Protein Pathway in Stress-induced Monoamine Oxidase A Expression

Grunewald

Johnson

et al. 2012

Journal of Biological Chemistry

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Background:The function of KLF11/TIEG2 under stressful conditions is undefined. Results: KLF11 increases brain MAO expression through its promoter and a chromatin partner, which can be enhanced by stress. Conclusion: This is the first elucidation of mechanisms underlying stress-induced KLF11-MAO up-regulation. Significance: This novel KLF11-MAO pathway may play an important role in stress-related brain disorders.

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Immunocytochemical localization of monoamine oxidases A and B in human peripheral tissues and brain.

Cited by 155 publications

References 28 publications

Interaction between a functional MAOA locus and childhood sexual abuse predicts alcoholism and antisocial personality disorder in adult women

Interaction between a functional MAOA locus and childhood sexual abuse predicts alcoholism and antisocial personality disorder in adult women

Dual Functions of Transcription Factors, Transforming Growth Factor-β-inducible Early Gene (TIEG)2 and Sp3, Are Mediated by CACCC Element and Sp1 Sites of Human Monoamine Oxidase (MAO) B Gene

Mechanistic Role for a Novel Glucocorticoid-KLF11 (TIEG2) Protein Pathway in Stress-induced Monoamine Oxidase A Expression

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