Please use this identifier to cite or link to this item: https://doi.org/10.1007/s12035-014-8974-4
Title: Inhibition of Excessive Monoamine Oxidase A/B Activity Protects Against Stress-induced Neuronal Death in Huntington Disease
Authors: Ooi, J
Hayden, M.R 
Pouladi, M.A 
Keywords: amine oxidase (flavin containing) isoenzyme A
amine oxidase (flavin containing) isoenzyme B
clorgyline
huntingtin
phenelzine
selegiline
amine oxidase (flavin containing)
dopamine
HTT protein, human
huntingtin
nerve protein
serotonin transporter
Slc6a4 protein, mouse
adult
aged
animal cell
Article
CAG repeat
cell stress
cell viability
child
clinical article
controlled study
corpus striatum
drug effect
enzyme activity
enzyme inhibition
epigenetics
female
human
human cell
Huntington chorea
male
middle aged
mouse
mutant
nerve cell differentiation
nerve cell necrosis
neural stem cell
neuroprotection
nonhuman
oxidative stress
pluripotent stem cell
preschool child
protein expression
skin fibroblast
young adult
animal
cell culture
cell death
disease model
Huntington chorea
metabolism
nerve cell
physiology
Animals
Cell Death
Cells, Cultured
Corpus Striatum
Disease Models, Animal
Dopamine
Humans
Huntingtin Protein
Huntington Disease
Mice
Monoamine Oxidase
Nerve Tissue Proteins
Neurons
Oxidative Stress
Serotonin Plasma Membrane Transport Proteins
Issue Date: 2015
Publisher: Humana Press Inc.
Citation: Ooi, J, Hayden, M.R, Pouladi, M.A (2015). Inhibition of Excessive Monoamine Oxidase A/B Activity Protects Against Stress-induced Neuronal Death in Huntington Disease. Molecular Neurobiology 52 (3) : 1850-1861. ScholarBank@NUS Repository. https://doi.org/10.1007/s12035-014-8974-4
Abstract: Monoamine oxidases (MAO) are important components of the homeostatic machinery that maintains the levels of monoamine neurotransmitters, including dopamine, in balance. Given the imbalance in dopamine levels observed in Huntington disease (HD), the aim of this study was to examine MAO activity in a mouse striatal cell model of HD and in human neural cells differentiated from control and HD patient-derived induced pluripotent stem cell (hiPSC) lines. We show that mouse striatal neural cells expressing mutant huntingtin (HTT) exhibit increased MAO expression and activity. We demonstrate using luciferase promoter assays that the increased MAO expression reflects enhanced epigenetic activation in striatal neural cells expressing mutant HTT. Using cellular stress paradigms, we further demonstrate that the increase in MAO activity in mutant striatal neural cells is accompanied by enhanced susceptibility to oxidative stress and impaired viability. Treatment of mutant striatal neural cells with MAO inhibitors ameliorated oxidative stress and improved cellular viability. Finally, we demonstrate that human HD neural cells exhibit increased MAO-A and MAO-B expression and activity. Altogether, this study demonstrates abnormal MAO expression and activity and suggests a potential use for MAO inhibitors in HD. © 2014, The Author(s).
Source Title: Molecular Neurobiology
URI: https://scholarbank.nus.edu.sg/handle/10635/175275
ISSN: 0893-7648
DOI: 10.1007/s12035-014-8974-4
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