α-Synuclein increases U251 cells vulnerability to hydrogen peroxide by disrupting calcium homeostasis

Zhengxin Ying; Fankai Lin; Weihong Gu; Yang Su; Abida Arshad; Hong Qing; Yulin Deng

doi:10.1007/s00702-011-0596-7

α-Synuclein increases U251 cells vulnerability to hydrogen peroxide by disrupting calcium homeostasis

Zhengxin Ying
, Fankai Lin
, Weihong Gu
, Yang Su
, Abida Arshad
, Hong Qing
, Yulin Deng^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

11 Citations (Scopus)

Abstract

Multiple system atrophy (MSA) is a progressive neurodegenerative disease characterized by glial cytoplasmic inclusions containing insoluble α-synuclein. Since Ca ²⁺ plays an important role in cell degeneration, [Ca ²⁺] _i in α-synuclein-overexpressed human glioma cells was analyzed by Fura-2 fluorometry. Overexpression of α-synuclein increased the basal level of [Ca ²⁺] _i, and a higher Ca ²⁺ response to hydrogen peroxide was further observed. The effect that α-synuclein overexpression caused U251 cells to be more vulnerable to hydrogen peroxide was eliminated by Ca ²⁺ chelator BAPTA-AM or transient receptor potential channels blocker SKF 96365 but not by L-type Ca ²⁺ channel blocker nimodipine. These findings suggest that the dysregulation of cellular Ca ²⁺ homeostasis caused by α-synuclein under oxidative stress may contribute to the glial cell death in MSA.

Original language	English
Pages (from-to)	1165-1172
Number of pages	8
Journal	Journal of Neural Transmission
Volume	118
Issue number	8
DOIs	https://doi.org/10.1007/s00702-011-0596-7
Publication status	Published - Aug 2011

Keywords

Calcium
Calcium channels
Multiple system atrophy
α-Synuclein

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This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1007/s00702-011-0596-7

Cite this

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title = "α-Synuclein increases U251 cells vulnerability to hydrogen peroxide by disrupting calcium homeostasis",

abstract = "Multiple system atrophy (MSA) is a progressive neurodegenerative disease characterized by glial cytoplasmic inclusions containing insoluble α-synuclein. Since Ca 2+ plays an important role in cell degeneration, [Ca 2+] i in α-synuclein-overexpressed human glioma cells was analyzed by Fura-2 fluorometry. Overexpression of α-synuclein increased the basal level of [Ca 2+] i, and a higher Ca 2+ response to hydrogen peroxide was further observed. The effect that α-synuclein overexpression caused U251 cells to be more vulnerable to hydrogen peroxide was eliminated by Ca 2+ chelator BAPTA-AM or transient receptor potential channels blocker SKF 96365 but not by L-type Ca 2+ channel blocker nimodipine. These findings suggest that the dysregulation of cellular Ca 2+ homeostasis caused by α-synuclein under oxidative stress may contribute to the glial cell death in MSA.",

keywords = "Calcium, Calcium channels, Multiple system atrophy, α-Synuclein",

author = "Zhengxin Ying and Fankai Lin and Weihong Gu and Yang Su and Abida Arshad and Hong Qing and Yulin Deng",

year = "2011",

month = aug,

doi = "10.1007/s00702-011-0596-7",

language = "English",

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pages = "1165--1172",

journal = "Journal of Neural Transmission",

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}

TY - JOUR

T1 - α-Synuclein increases U251 cells vulnerability to hydrogen peroxide by disrupting calcium homeostasis

AU - Ying, Zhengxin

AU - Lin, Fankai

AU - Gu, Weihong

AU - Su, Yang

AU - Arshad, Abida

AU - Qing, Hong

AU - Deng, Yulin

PY - 2011/8

Y1 - 2011/8

N2 - Multiple system atrophy (MSA) is a progressive neurodegenerative disease characterized by glial cytoplasmic inclusions containing insoluble α-synuclein. Since Ca 2+ plays an important role in cell degeneration, [Ca 2+] i in α-synuclein-overexpressed human glioma cells was analyzed by Fura-2 fluorometry. Overexpression of α-synuclein increased the basal level of [Ca 2+] i, and a higher Ca 2+ response to hydrogen peroxide was further observed. The effect that α-synuclein overexpression caused U251 cells to be more vulnerable to hydrogen peroxide was eliminated by Ca 2+ chelator BAPTA-AM or transient receptor potential channels blocker SKF 96365 but not by L-type Ca 2+ channel blocker nimodipine. These findings suggest that the dysregulation of cellular Ca 2+ homeostasis caused by α-synuclein under oxidative stress may contribute to the glial cell death in MSA.

AB - Multiple system atrophy (MSA) is a progressive neurodegenerative disease characterized by glial cytoplasmic inclusions containing insoluble α-synuclein. Since Ca 2+ plays an important role in cell degeneration, [Ca 2+] i in α-synuclein-overexpressed human glioma cells was analyzed by Fura-2 fluorometry. Overexpression of α-synuclein increased the basal level of [Ca 2+] i, and a higher Ca 2+ response to hydrogen peroxide was further observed. The effect that α-synuclein overexpression caused U251 cells to be more vulnerable to hydrogen peroxide was eliminated by Ca 2+ chelator BAPTA-AM or transient receptor potential channels blocker SKF 96365 but not by L-type Ca 2+ channel blocker nimodipine. These findings suggest that the dysregulation of cellular Ca 2+ homeostasis caused by α-synuclein under oxidative stress may contribute to the glial cell death in MSA.

KW - Calcium

KW - Calcium channels

KW - Multiple system atrophy

KW - α-Synuclein

UR - https://www.scopus.com/pages/publications/80051595745

U2 - 10.1007/s00702-011-0596-7

DO - 10.1007/s00702-011-0596-7

M3 - Article

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AN - SCOPUS:80051595745

SN - 0300-9564

VL - 118

SP - 1165

EP - 1172

JO - Journal of Neural Transmission

JF - Journal of Neural Transmission

IS - 8

ER -

α-Synuclein increases U251 cells vulnerability to hydrogen peroxide by disrupting calcium homeostasis

Abstract

Keywords

UN SDGs

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