A comparative study of the expression of monoamine oxidase-A and -B mRNA and protein in non-CNS human tissues

Sivasubramaniam, Shiva; Finch, Cheryl C.; Rodrı́guez, Manuel J.; Mahy, Nicole; Billett, E. Ellen

doi:10.1007/s00441-003-0765-6

Cited by 69 publications

(54 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…MAO-A activity is central to the enhanced norepinephrine catabolism present in the failing hearts. Differently from MAO-A, the possible pathogenetic contribution of MAO-B to heart failure has been completely neglected despite the fact that this isoenzyme is highly expressed in mouse and human hearts (15,27,36) and its pivotal role in dopamine degradation in the brain of human and other primates (7). Here we report that the genetic ablation of MAO-B favors the maintenance of stable concentric hypertrophy with maintained LV function, preventing the transition to overt LV dilation and pump failure in pressure overloaded hearts.…”

Section: Impact Of Mao-b Deletion On LV Adaptation To Chronic Stress mentioning

confidence: 99%

“…Until now, the attention has been focused on MAO-A, since it is the predominant isoform expressed in rat heart (15,27,36). However, MAO-B is highly abundant in the myocardium of species, such as mice and humans (15,36).…”

mentioning

confidence: 99%

“…However, MAO-B is highly abundant in the myocardium of species, such as mice and humans (15,36). Notwithstanding, virtually nothing is known about its possible influence on myocardial structure and function.…”

mentioning

confidence: 99%

See 2 more Smart Citations

Monoamine Oxidase B Prompts Mitochondrial and Cardiac Dysfunction in Pressure Overloaded Hearts

Kaludercic

Carpi

Nagayama

et al. 2014

Antioxidants & Redox Signaling

146

139

View full text Add to dashboard Cite

Aims: Monoamine oxidases (MAOs) are mitochondrial flavoenzymes responsible for neurotransmitter and biogenic amines catabolism. MAO-A contributes to heart failure progression via enhanced norepinephrine catabolism and oxidative stress. The potential pathogenetic role of the isoenzyme MAO-B in cardiac diseases is currently unknown. Moreover, it is has not been determined yet whether MAO activation can directly affect mitochondrial function. Results: In wild type mice, pressure overload induced by transverse aortic constriction (TAC) resulted in enhanced dopamine catabolism, left ventricular (LV) remodeling, and dysfunction. Conversely, mice lacking MAO-B (MAO-B -/ -) subjected to TAC maintained concentric hypertrophy accompanied by extracellular signal regulated kinase (ERK)1/2 activation, and preserved LV function, both at early (3 weeks) and late stages (9 weeks). Enhanced MAO activation triggered oxidative stress, and dropped mitochondrial membrane potential in the presence of ATP synthase inhibitor oligomycin both in neonatal and adult cardiomyocytes. The MAO-B inhibitor pargyline completely offset this change, suggesting that MAO activation induces a latent mitochondrial dysfunction, causing these organelles to hydrolyze ATP. Moreover, MAO-dependent aldehyde formation due to inhibition of aldehyde dehydrogenase 2 activity also contributed to alter mitochondrial bioenergetics. Innovation: Our study unravels a novel role for MAO-B in the pathogenesis of heart failure, showing that both MAO-driven reactive oxygen species production and impaired aldehyde metabolism affect mitochondrial function. Conclusion: Under conditions of chronic hemodynamic stress, enhanced MAO-B activity is a major determinant of cardiac structural and functional disarrangement. Both increased oxidative stress and the accumulation of aldehyde intermediates are likely liable for these adverse morphological and mechanical changes by directly targeting mitochondria. Antioxid. Redox Signal. 20, 267-280.

show abstract

Section: Impact Of Mao-b Deletion On LV Adaptation To Chronic Stress mentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Monoamine Oxidase B Prompts Mitochondrial and Cardiac Dysfunction in Pressure Overloaded Hearts

Kaludercic

Carpi

Nagayama

et al. 2014

Antioxidants & Redox Signaling

146

139

View full text Add to dashboard Cite

show abstract

“…The oxidative degradation catalyzed by MAO produces free radicals and may thus be involved in the neurodegenerative process (73,74). In the CNS, the MAO-A isoform appears to be present mainly in catecholaminergic neurons, whereas the MAO-B form is primarily located in the glia and in serotonergic neurons (49).…”

Section: Alterations In Mao Levels In the Brains Of Patients With Admentioning

confidence: 99%

Monoamine oxidase inhibitors: Promising therapeutic agents for Alzheimer’s disease (Review)

Cai

2014

Molecular Medicine Reports

180

View full text Add to dashboard Cite

Abstract. Activated monoamine oxidase (MAO) has a critical role in the pathogenesis of Alzheimer's disease (AD), including the formation of amyloid plaques from amyloid β peptide (Aβ) production and accumulation, formation of neurofibrillary tangles, and cognitive impairment via the destruction of cholinergic neurons and disorder of the cholinergic system. Several studies have indicated that MAO inhibitors improve cognitive deficits and reverse Aβ pathology by modulating proteolytic cleavage of amyloid precursor protein and decreasing Aβ protein fragments. Thus, MAO inhibitors may be considered as promising therapeutic agents for AD.

show abstract

“…MAO-A is present in the myocardium of diverse species from rodents to humans (73,74). The heart contains a large amount of MAO-A (75,76) and its role in the regulation of cardiac function critically involves NE concentrations (77,78).…”

Section: The Role Of Mao-a In the Pathophysiology And Therapeutics Ofmentioning

confidence: 99%

Abnormal function of monoamine oxidase-A in comorbid major depressive disorder and cardiovascular disease: Pathophysiological and therapeutic implications (Review)

Machado‐Vieira

Mallinger

2012

Mol Med Report

View full text Add to dashboard Cite

Abstract. The association between major depressive disorder (MDD) and cardiovascular disease (CVD) is among the best described medical comorbidities. The presence of MDD increases the risk of cardiac admissions and mortality and increases healthcare costs in patients with CVD, and similarly, CVD affects the course and outcome of MDD. The potential shared biological mechanisms involved in these comorbid conditions are not well known. However, the enzyme monoamine oxidase-A (MAO-A), which has a key role in the degradation of catecholamines, has been associated with the pathophysiology and therapeutics of both MDD and CVD. Increased MAO-A activity results in the dysregulation of downstream targets of this enzyme and thus affects the pathophysiology of the two diseases. These deleterious effects include altered noradrenaline turnover, with a direct elevation in oxidative stress parameters, as well as increased platelet activity and cytokine levels. These effects were shown to be reversed by MAO inhibitors. Here, a model describing a key role for the MAO-A in comorbid MDD and CVD is proposed, with focus on the shared pathophysiological mechanisms and the potential therapeutic relevance of agents targeting this enzyme.

show abstract

A comparative study of the expression of monoamine oxidase-A and -B mRNA and protein in non-CNS human tissues

Cited by 69 publications

References 34 publications

Monoamine Oxidase B Prompts Mitochondrial and Cardiac Dysfunction in Pressure Overloaded Hearts

Monoamine Oxidase B Prompts Mitochondrial and Cardiac Dysfunction in Pressure Overloaded Hearts

Monoamine oxidase inhibitors: Promising therapeutic agents for Alzheimer’s disease (Review)

Abnormal function of monoamine oxidase-A in comorbid major depressive disorder and cardiovascular disease: Pathophysiological and therapeutic implications (Review)

Contact Info

Product

Resources

About