Title: High levels of Mn²⁺ inhibit secretory pathway Ca²⁺/Mn²⁺-ATPase (SPCA) activity and cause Golgi fragmentation in neurons and glia
Authors: Sepúlveda, M Rosario ×
Wuytack, Frank
Mata, Ana M #
Issue Date: Dec-2012
Publisher: Raven Press
Series Title: Journal of Neurochemistry vol:123 issue:5 pages:824-836
Article number: 10.1111/j.1471-4159.2012.07888.x
Abstract: Excess Mn(2+) in humans causes a neurological disorder known as manganism, which shares symptoms with Parkinson's disease. However, the cellular mechanisms underlying Mn(2+) -neurotoxicity and the involvement of Mn(2+) -transporters in cellular homeostasis and repair are poorly understood and require further investigation. In this work, we have analyzed the effect of Mn(2+) on neurons and glia from mice in primary cultures. Mn(2+) overload compromised survival of both cell types, specifically affecting cellular integrity and Golgi organization, where the secretory pathway Ca(2+) /Mn(2+) -ATPase is localized. This ATP-driven Mn(2+) transporter might take part in Mn(2+) accumulation/detoxification at low loads of Mn(2+) , but its ATPase activity is inhibited at high concentration of Mn(2+) . Glial cells appear to be significantly more resistant to this toxicity than neurons and their presence in cocultures provided some protection to neurons against degeneration induced by Mn(2+) . Interestingly, the Mn(2+) toxicity was partially reversed upon Mn(2+) removal by wash out or by the addition of EDTA as a chelating agent, in particular in glial cells. These studies provide data on Mn(2+) neurotoxicity and may contribute to explore new therapeutic approaches for reducing Mn(2+) poisoning.
ISSN: 0022-3042
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Laboratory of Cellular Transport Systems
× corresponding author
# (joint) last author

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