NDLI: Copper modulates the large dense core vesicle secretory pathway in PC12 cells

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Inside back cover

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Metallomics Vol - 5 Issue - 5

Metallomics Vol - 5 Issue - 4

Metallomics Vol - 5 Issue - 3

Metallomics Vol - 5 Issue - 2

Copper modulates the large dense core vesicle secretory pathway in PC12 cells

Content Provider	Royal Society of Chemistry (RSC)
Author	Duffield, Michael D. Crouch, Peter J. Volitakis, Irene Lidgerwood, Grace E. Liddell, Jeffrey R. Donnelly, Paul S. Parker, Sarah J. Duncan, Clare Caragounis, Aphrodite Raghupathi, Ravinarayan White, Anthony R. Paterson, Brett M. Keating, Damien J. Meyerowitz, Jodi Camakaris, James Grubman, Alexandra Cappai, Roberto Bica, Laura
Copyright Year	2013
Abstract	Copper (Cu) is an essential biometal involved in a number of cell functions. Abnormal Cu homeostasis has been identified as a major factor in a number of neurodegenerative disorders. However, little is known about how cells of brain origin maintain Cu homeostasis and in particular, how they respond to an elevated Cu environment. Understanding these processes is essential to obtaining a greater insight into the pathological changes in neurodegeneration and ageing. Although previous studies have shown that Cu in neurons can be associated with synaptic function, there is little understanding of how Cu modulates the regulated secretory vesicle pathways in these cells. In this study, we examined the effect of elevated intracellular Cu on proteins associated with the regulated secretory vesicle pathway in NGF-differentiated PC12 cells that exhibit neuronal-like properties. Increasing intracellular Cu with a cell-permeable Cu-complex (CuII(gtsm)) resulted in increased expression of synaptophysin and robust translocation of this and additional vesicular proteins from synaptic-like microvesicle (SLMV) fractions to chromogranin-containing putative large dense core vesicle (LDCV) fractions in density gradient preparations. The LDCV fractions also contained substantially elevated Cu levels upon treatment of cells with CuII(gtsm). Expression of the H+ pump, V-ATPase, which is essential for vesicle maturation, was increased in Cu-treated cells while inhibition of V-ATPase prevented translocation of synaptophysin to LDCV fractions. Cu treatment was found to inhibit release of LDCVs in chromaffin cells due to reduced Ca2+-mediated vesicle exocytosis. Our findings demonstrate that elevated Cu can modulate LDCV metabolism potentially resulting in sequestration of Cu in this vesicle pool.
Starting Page	700
Ending Page	714
Page Count	15
File Format	HTM / HTML PDF
ISSN	17565901
Volume Number	5
Issue Number	6
Journal	Metallomics
DOI	10.1039/c3mt20231c
Language	English
Publisher	Royal Society of Chemistry
Access Restriction	Open
Subject Keyword	Synaptophysin Cu V-ATPase Neurodegeneration PC12 cell line Homeostasis Proton Chromaffin cell Exocytosis Metabolism
Content Type	Text
Resource Type	Article
Subject	Chemistry Medicine Metals and Alloys Biochemistry Biomaterials Biophysics

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