Estrogen modulation of catecholamine synthesis and monoamine oxidase A activity in the human neuroblastoma cell line SK-ER3

Ma, Zhiqing; Bondiolotti, Gianpietro; Olasmaa, Marjut; Violani, Elisabetta; Patrone, Cesare; Picotti, G. B.; Maggi, Adriana

doi:10.1016/0960-0760(93)90076-9

Cited by 31 publications

(17 citation statements)

References 9 publications

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“…The cause for the possible gender effect on this polymorphism is unknown. One possible explanation comes from the evidence that, in the transfected cell line, MAOA activity is reduced by estrogen treatment (Ma et al, 1993). Furthermore, the MAOA is on the X chromosome.…”

Section: Discussionmentioning

confidence: 99%

Association Study of a Monoamine Oxidase A Gene Promoter Polymorphism with Major Depressive Disorder and Antidepressant Response

Yu¹,

Tsai

Hong

et al. 2005

Neuropsychopharmacol

161

121

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Monoamine oxidase A (MAOA), a mitochondrial enzyme involved in the degradation of biogenic amines, may be implicated in the pathogenesis of major depressive disorder (MDD) and be related to the therapeutic effects of antidepressants. To elucidate a genetic predisposition of MDD, we studied a variable-number-tandem-repeat (VNTR) polymorphism in the promoter region of the MAOA gene in a Chinese population of 230 MDD patients and 217 controls. We also examined the association of this polymorphism and antidepressant therapeutic response in the MDD patients who underwent a 4-week fluoxetine treatment. Our results showed a significantly increased frequency of 4-repeat (4R) allele in MDD patients, especially in the female population. Furthermore, MDD female patients who were 3R homozygotes had a significantly better response to 4-week fluoxetine treatment when compared to 4R carriers (p ¼ 0.024), but there was a nonsignificant difference found in male patients (p ¼ 0.081). Since the 4R allele transcribed 2-10 times more efficiently than those with 3R allele, our findings suggest that the MAOA-uVNTR may be involved in the pathogenesis of MDD and the antidepressant therapeutic mechanisms in Chinese population, and that there may be a gender effect in this association.

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Section: Discussionmentioning

confidence: 99%

Association Study of a Monoamine Oxidase A Gene Promoter Polymorphism with Major Depressive Disorder and Antidepressant Response

Yu¹,

Tsai

Hong

et al. 2005

Neuropsychopharmacol

161

121

View full text Add to dashboard Cite

show abstract

“…Given the functions of MAO-A, the present study argues that several types of processes that contribute to pathological mood are enhanced in PPD. MAO-A V T is an index of MAO-A level (Tong et al, 2013;Ginovart et al, 2006) and the changes in latter are strongly implicated in the effects of hormonal influences on the MAO-A activity (Nelson et al, 1979;Edelstein and Breakefield, 1986;Saura et al, 1992;Ma et al, 1993;Smith et al, 2004). MAO-A metabolizes monoamines such as serotonin, norepinephrine, and dopamine, creates reactive oxygen species such as hydrogen peroxide (H 2 O 2 ), thereby promoting a pro-oxidant state (Youdim et al, 2006), suggesting that enhanced monoamine metabolism and a pro-oxidant state may be present during PPD.…”

Section: Discussionmentioning

confidence: 99%

Relationship of Monoamine Oxidase-A Distribution Volume to Postpartum Depression and Postpartum Crying

Sacher

Rekkas

Wilson

et al. 2014

Neuropsychopharmacol

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Postpartum depression (PPD) has a prevalence rate of 13% and a similarly high proportion of women report a subclinical state of one or more major depressive episode symptoms. The aim was to investigate whether monoamine oxidase-A (MAO-A) V T , an index of MAO-A density, is increased in the prefrontal and anterior cingulate cortex (PFC and ACC), during PPD or when a PPD spectrum symptom, greater predisposition to crying, is present. MAO-A is an enzyme that increases in density after estrogen decline, and has several functions including creating oxidative stress, influencing apoptosis and monoamine metabolism. Fifty-seven women were recruited including 15 first-onset, antidepressant naive, PPD subjects, 12 postpartum healthy who cry due to sad mood, 15 asymptomatic postpartum healthy women, and 15 healthy women not recently pregnant. Each underwent [11 C]-harmine positron emission tomography scanning to measure MAO-A V T . Both PPD and greater predisposition to crying were associated with greater MAO-A V T in the PFC and ACC (multivariate analysis of variance (MANOVA), group effect, F 21,135 ¼ 1.856; p ¼ 0.019; mean combined region elevation 21% and 14% in PPD and crying groups, respectively, relative to postpartum asymptomatic). Greater MAO-A V T in the PFC and ACC represents a new biomarker in PPD, and the PPD symptom of predisposition to crying. Novel strategies for preventing PPD (and some PPD symptoms) may be possible by avoiding environmental conditions that elevate MAO-A level and enhancing conditions that normalize MAO-A level. These findings also argue for clinical trials in PPD with the newer, well-tolerated MAO-A inhibitor antidepressants.

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“…However, we currently do not have information concerning possible E2 regulation in the blood, although reports in the literature suggested that there are E2-regulated genes in blood and that, for example, MAO-A may be a candidate for an E2-regulated gene which could be assayed in human blood samples. (48).…”

Section: The Marker Genesmentioning

confidence: 99%

“…However, the required concentrations are so high that the effects may not be ER mediated; this is similar to what has been observed in SK-N-BE/SK-ER3 cells, in which the observed effects of tamoxifen apparently are independent of the presence of ERa. Unfortunately, the possible expression of ER,I has not been investigated in the SK-N-BE cells, although the lack of E2 response indicates that neither receptor subtype is present (48,49).…”

Section: The Marker Genesmentioning

confidence: 99%

“…The expression level of pS2 mRNA is a widely used indicator of estrogenicity, and the translation product of pS2 mRNA is also induced in MCF-7 cells in response to estrogen (37). The 9 kDa encoded pS2 protein belongs to the trefoil family of peptides (48)(49)(50). In vivo assays have been conducted because there seems to be a correlation between mood changes and estradiol levels that may be mediated through the activity of monoamine oxidases (51)(52)(53).…”

Section: The Marker Genesmentioning

confidence: 99%

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Assaying Estrogenicity by Quantitating the Expression Levels of Endogenous Estrogen-Regulated Genes

Jørgensen¹,

Vendelbo²,

Skakkebæk³

et al. 2000

Environmental Health Perspectives

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Scientific edence suggests that humans and wildlife speces may experience adverse health consequences from exposure to environmental chemicals that interact with the endocrine system. Reliable short-term assays are needed to identifr hormone-dismpting chemicals. In this study we demonstrate that the estrogenic activity of a chemical can be evaluated by assaying induction or repression of endogenous estrogen-regulated 'marker genes" in human breast cancer MCF-7 cells. We induded four marker genes in the assay -pS2, transforming growth factor P3 (TGa933), monoamine oxidase A, and ecl-antichymotrypsin-and we evaluated estrogeniic acivity for 17P-estradiol (E2), diethylstilbestrol, ci-zearalanol, nonylphenol, genistein, methoxychlor, endosulphan, o,p-DDE, bisphenol A, dibutylphthalate, 4-hydoxy tamoxifn, and ICI 182.780. All four marker genes responded strongly to the three high-potency estrogens (E29diethylstilbestol, and -earalanol), whereas the potency of the other chemicals was 103-to 106-fold lower than that of E2. There were some maker gene-dependent differences in the relative potencies of the tested chemicals. TG$P3 was equally sensitive to the three high-potency estrogens, whereas the sensitivity to oc-zearalanol was approximately 10-fold lower than the sensitivity to E2 and diethyistilbestrol when assayed with the other three marker genes. TIhe potency of nonylphenol was equal to that of genistein when assayed with pS2 and TG1f3, but 10-to 100-fold higherilower with monoamine oxidase A and al-antichymotypsin, respectively. The results are in agreement with results obtained by other methods and suggest that an assay based on endogenous gene expression may offer an attractive alternative to other E-SCREEN methods.

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Estrogen modulation of catecholamine synthesis and monoamine oxidase A activity in the human neuroblastoma cell line SK-ER3

Cited by 31 publications

References 9 publications

Association Study of a Monoamine Oxidase A Gene Promoter Polymorphism with Major Depressive Disorder and Antidepressant Response

Association Study of a Monoamine Oxidase A Gene Promoter Polymorphism with Major Depressive Disorder and Antidepressant Response

Relationship of Monoamine Oxidase-A Distribution Volume to Postpartum Depression and Postpartum Crying

Assaying Estrogenicity by Quantitating the Expression Levels of Endogenous Estrogen-Regulated Genes

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