Unveiling the Role of DJ-1 Protein in Vesicular Storage and Release of Catecholamine with Nano/Micro-Tip Electrodes.

Abstract

DJ-1 protein deficiency caused by PARK7 gene mutation has been suggested to closely relate to Parkinson's disease (PD), mainly through the attenuation D2 dopamine receptor activity in mice; however, whether or how it affects the vesicular storage and exocytosis of neurochemicals remains unclear. By using electrochemical methods at a single vesicle/cell level with nano/micro-tip electrodes, we for the first time find that DJ-1 protein deficiency caused by PARK7 gene knockout (KO) in mice has little effect on vesicular catecholamine content but significantly prolongs the exocytotic events, especially the closing time of exocytotic fusion pores. Further studies suggest the inhibition of α-synuclein aggregation by DJ-1 protein might be one way that DJ-1 protein acts on neurotransmission. This finding offers the first direct link between DJ-1 protein deficiency and vesicular chemical storage and release of chemicals, providing a new chemical insight into the pathology of PD caused by PARK7 gene mutation.

• Authors: Qingwei Yue, Xianchan Li, Fei Wu, Wenliang Ji, Yue Zhang, Ping Yu, Meining Zhang, Wenjie Ma, Ming Wang, Lanqun Mao
• Journal: Angewandte Chemie (International ed. in English) (Angew Chem Int Ed Engl) Vol. 59 Issue 27 Pg. 11061-11065 (06 26 2020) ISSN: 1521-3773 [Electronic] Germany
• PMID: 32249515 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: © 2020 Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim.

Chemical References

• Catecholamines
• PARK7 protein, mouse
• Protein Deglycase DJ-1

Topics

• Animals
• Catecholamines (metabolism)
• Electrodes
• Mice
• Mice, Knockout
• Mutation
• Nanotechnology
• Protein Deglycase DJ-1 (genetics, physiology)
• Synaptic Transmission (physiology)