Voltage-Gated Potassium Channel KV1.5 Protects against MPP+ Mediated Neurotoxicity in PC12 Cells

Chao Qu; Xiao-Zhen Fu; Chao Han; Qian Chen; Yan Liu; Xiao-bo Wang; Rong-Gang Xi; Jing Liu; Wei Zou

doi:doi:10.11648/j.ab.20140206.14

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Voltage-Gated Potassium Channel KV1.5 Protects against MPP+ Mediated Neurotoxicity in PC12 Cells

Chao Qu, Xiao-Zhen Fu, Chao Han, Qian Chen, Yan Liu, Xiao-bo Wang, Rong-Gang Xi, Jing Liu, Wei Zou

Published in Advances in Biochemistry (Volume 2, Issue 6)

Received: 4 December 2014 Accepted: 22 December 2014 Published: 31 December 2014

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Abstract

Background: Parkinson’s disease (PD) is the second most common neurodegenerative disease and afflicts almost 1.8% of over 65-year-old group in the world. Epidemiological projections showed that the incidence of PD was increasing continuously each year, with a wider age range as well. A large number of studies indicated that voltage-gated potassium channel (Kv) played significant roles in cellular signaling in both excitable and non-excitable cells. What’s more, Kv was also ubiquitously expressed in neurons and participated in signaling pathway in neurons. Kv1.5 (encoded by KCNA5) is an important voltage-gated K+ channel, which is not only necessary for critical processes such as cell proliferation and apoptosis but ubiquitously expressed in neurons. Recent studies reported that PD clinical drugs could inhibit the expression of Kv1.5. To determine the mechanisms by which Kv1.5 protects against MPP+ mediated neurotoxicity in PC12 cells. Materials and Methods: Knockdown of Kv1.5 model was established with pSINsi-hU6- Kv1.5 treated by the RNAi method in PC12. MTT, and Western Blot were used to detect the influence of Kv1.5 on PC12 proliferation, and the effect of Kv1.5 on PC12 apoptosis after MPP+ treatment in vitro. Results: 1) Knockdown and overexpression of Kv1.5 participated in PC12 proliferation. Transiently over-expressed Kv1.5 could boost the survival rate of PC12, while transiently knockdown of Kv1.5 inhibited PC12 proliferation. 2) The effect of Kv1.5 on PC12 proliferation was through PI3K/Akt signaling pathway. Over-expressed Kv1.5 could induce the activation of Akt, and Bcl-2 expression in PC12; Knockdown of Kv1.5 in PC12 inhibited the activation of Akt, Bcl-2 expression, and promoted MAPK phosphorylation. 3) Over-expressed Kv1.5 could significantly prevent PC12 from apoptosis induced by MPP+ via activating Akt pathway and increasing Bcl-2 expression; Knockdown of Kv1.5 was more sensitive than its control counterpart when treated with MPP+ for 24 h. Conclusion: Kv1.5 could hinder MPP+ neurotoxicity to PC12 by PI3K/Akt signaling pathway.

Published in	Advances in Biochemistry (Volume 2, Issue 6)
DOI	10.11648/j.ab.20140206.14
Page(s)	103-108
Creative Commons	This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.
Copyright	Copyright © The Author(s), 2014. Published by Science Publishing Group

Keywords

PC12, Kv1.5, MPP+, PD, PI3K/Akt

References

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APA Style

Chao Qu, Xiao-Zhen Fu, Chao Han, Qian Chen, Yan Liu, et al. (2014). Voltage-Gated Potassium Channel KV1.5 Protects against MPP+ Mediated Neurotoxicity in PC12 Cells. Advances in Biochemistry, 2(6), 103-108. https://doi.org/10.11648/j.ab.20140206.14

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ACS Style

Chao Qu; Xiao-Zhen Fu; Chao Han; Qian Chen; Yan Liu, et al. Voltage-Gated Potassium Channel KV1.5 Protects against MPP+ Mediated Neurotoxicity in PC12 Cells. Adv. Biochem. 2014, 2(6), 103-108. doi: 10.11648/j.ab.20140206.14

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AMA Style

Chao Qu, Xiao-Zhen Fu, Chao Han, Qian Chen, Yan Liu, et al. Voltage-Gated Potassium Channel KV1.5 Protects against MPP+ Mediated Neurotoxicity in PC12 Cells. Adv Biochem. 2014;2(6):103-108. doi: 10.11648/j.ab.20140206.14

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@article{10.11648/j.ab.20140206.14,
  author = {Chao Qu and Xiao-Zhen Fu and Chao Han and Qian Chen and Yan Liu and Xiao-bo Wang and Rong-Gang Xi and Jing Liu and Wei Zou},
  title = {Voltage-Gated Potassium Channel KV1.5 Protects against MPP+ Mediated Neurotoxicity in PC12 Cells},
  journal = {Advances in Biochemistry},
  volume = {2},
  number = {6},
  pages = {103-108},
  doi = {10.11648/j.ab.20140206.14},
  url = {https://doi.org/10.11648/j.ab.20140206.14},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ab.20140206.14},
  abstract = {Background: Parkinson’s disease (PD) is the second most common neurodegenerative disease and afflicts almost 1.8% of over 65-year-old group in the world. Epidemiological projections showed that the incidence of PD was increasing continuously each year, with a wider age range as well. A large number of studies indicated that voltage-gated potassium channel (Kv) played significant roles in cellular signaling in both excitable and non-excitable cells. What’s more, Kv was also ubiquitously expressed in neurons and participated in signaling pathway in neurons. Kv1.5 (encoded by KCNA5) is an important voltage-gated K+ channel, which is not only necessary for critical processes such as cell proliferation and apoptosis but ubiquitously expressed in neurons. Recent studies reported that PD clinical drugs could inhibit the expression of Kv1.5. To determine the mechanisms by which Kv1.5 protects against MPP+ mediated neurotoxicity in PC12 cells. Materials and Methods: Knockdown of Kv1.5 model was established with pSINsi-hU6- Kv1.5 treated by the RNAi method in PC12. MTT, and Western Blot were used to detect the influence of Kv1.5 on PC12 proliferation, and the effect of Kv1.5 on PC12 apoptosis after MPP+ treatment in vitro. Results: 1) Knockdown and overexpression of Kv1.5 participated in PC12 proliferation. Transiently over-expressed Kv1.5 could boost the survival rate of PC12, while transiently knockdown of Kv1.5 inhibited PC12 proliferation. 2) The effect of Kv1.5 on PC12 proliferation was through PI3K/Akt signaling pathway. Over-expressed Kv1.5 could induce the activation of Akt, and Bcl-2 expression in PC12; Knockdown of Kv1.5 in PC12 inhibited the activation of Akt, Bcl-2 expression, and promoted MAPK phosphorylation. 3) Over-expressed Kv1.5 could significantly prevent PC12 from apoptosis induced by MPP+ via activating Akt pathway and increasing Bcl-2 expression; Knockdown of Kv1.5 was more sensitive than its control counterpart when treated with MPP+ for 24 h. Conclusion: Kv1.5 could hinder MPP+ neurotoxicity to PC12 by PI3K/Akt signaling pathway.},
 year = {2014}
}

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TY  - JOUR
T1  - Voltage-Gated Potassium Channel KV1.5 Protects against MPP+ Mediated Neurotoxicity in PC12 Cells
AU  - Chao Qu
AU  - Xiao-Zhen Fu
AU  - Chao Han
AU  - Qian Chen
AU  - Yan Liu
AU  - Xiao-bo Wang
AU  - Rong-Gang Xi
AU  - Jing Liu
AU  - Wei Zou
Y1  - 2014/12/31
PY  - 2014
N1  - https://doi.org/10.11648/j.ab.20140206.14
DO  - 10.11648/j.ab.20140206.14
T2  - Advances in Biochemistry
JF  - Advances in Biochemistry
JO  - Advances in Biochemistry
SP  - 103
EP  - 108
PB  - Science Publishing Group
SN  - 2329-0862
UR  - https://doi.org/10.11648/j.ab.20140206.14
AB  - Background: Parkinson’s disease (PD) is the second most common neurodegenerative disease and afflicts almost 1.8% of over 65-year-old group in the world. Epidemiological projections showed that the incidence of PD was increasing continuously each year, with a wider age range as well. A large number of studies indicated that voltage-gated potassium channel (Kv) played significant roles in cellular signaling in both excitable and non-excitable cells. What’s more, Kv was also ubiquitously expressed in neurons and participated in signaling pathway in neurons. Kv1.5 (encoded by KCNA5) is an important voltage-gated K+ channel, which is not only necessary for critical processes such as cell proliferation and apoptosis but ubiquitously expressed in neurons. Recent studies reported that PD clinical drugs could inhibit the expression of Kv1.5. To determine the mechanisms by which Kv1.5 protects against MPP+ mediated neurotoxicity in PC12 cells. Materials and Methods: Knockdown of Kv1.5 model was established with pSINsi-hU6- Kv1.5 treated by the RNAi method in PC12. MTT, and Western Blot were used to detect the influence of Kv1.5 on PC12 proliferation, and the effect of Kv1.5 on PC12 apoptosis after MPP+ treatment in vitro. Results: 1) Knockdown and overexpression of Kv1.5 participated in PC12 proliferation. Transiently over-expressed Kv1.5 could boost the survival rate of PC12, while transiently knockdown of Kv1.5 inhibited PC12 proliferation. 2) The effect of Kv1.5 on PC12 proliferation was through PI3K/Akt signaling pathway. Over-expressed Kv1.5 could induce the activation of Akt, and Bcl-2 expression in PC12; Knockdown of Kv1.5 in PC12 inhibited the activation of Akt, Bcl-2 expression, and promoted MAPK phosphorylation. 3) Over-expressed Kv1.5 could significantly prevent PC12 from apoptosis induced by MPP+ via activating Akt pathway and increasing Bcl-2 expression; Knockdown of Kv1.5 was more sensitive than its control counterpart when treated with MPP+ for 24 h. Conclusion: Kv1.5 could hinder MPP+ neurotoxicity to PC12 by PI3K/Akt signaling pathway.
VL  - 2
IS  - 6
ER  -

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Author Information

Chao Qu

College of Life Science, Liaoning Normal University, Dalian 116081, China
Xiao-Zhen Fu

College of Life Science, Liaoning Normal University, Dalian 116081, China
Chao Han

College of Life Science, Liaoning Normal University, Dalian 116081, China
Qian Chen

College of Life Science, Liaoning Normal University, Dalian 116081, China
Yan Liu

College of Life Science, Liaoning Normal University, Dalian 116081, China
Xiao-bo Wang

The 210th Hospital of PLA, Dalian 116015, Liaoning, Province, China
Rong-Gang Xi

The 210th Hospital of PLA, Dalian 116015, Liaoning, Province, China
Jing Liu

Centre for Regenerative Medicine, First Affiliated Hospital of Dalian Medical University, Dalian 116011, Liaoning Province, China
Wei Zou

College of Life Science, Liaoning Normal University, Dalian 116081, China

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APA Style

Chao Qu, Xiao-Zhen Fu, Chao Han, Qian Chen, Yan Liu, et al. (2014). Voltage-Gated Potassium Channel KV1.5 Protects against MPP+ Mediated Neurotoxicity in PC12 Cells. Advances in Biochemistry, 2(6), 103-108. https://doi.org/10.11648/j.ab.20140206.14

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ACS Style

Chao Qu; Xiao-Zhen Fu; Chao Han; Qian Chen; Yan Liu, et al. Voltage-Gated Potassium Channel KV1.5 Protects against MPP+ Mediated Neurotoxicity in PC12 Cells. Adv. Biochem. 2014, 2(6), 103-108. doi: 10.11648/j.ab.20140206.14

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AMA Style

Chao Qu, Xiao-Zhen Fu, Chao Han, Qian Chen, Yan Liu, et al. Voltage-Gated Potassium Channel KV1.5 Protects against MPP+ Mediated Neurotoxicity in PC12 Cells. Adv Biochem. 2014;2(6):103-108. doi: 10.11648/j.ab.20140206.14

Copy | Download

@article{10.11648/j.ab.20140206.14,
  author = {Chao Qu and Xiao-Zhen Fu and Chao Han and Qian Chen and Yan Liu and Xiao-bo Wang and Rong-Gang Xi and Jing Liu and Wei Zou},
  title = {Voltage-Gated Potassium Channel KV1.5 Protects against MPP+ Mediated Neurotoxicity in PC12 Cells},
  journal = {Advances in Biochemistry},
  volume = {2},
  number = {6},
  pages = {103-108},
  doi = {10.11648/j.ab.20140206.14},
  url = {https://doi.org/10.11648/j.ab.20140206.14},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ab.20140206.14},
  abstract = {Background: Parkinson’s disease (PD) is the second most common neurodegenerative disease and afflicts almost 1.8% of over 65-year-old group in the world. Epidemiological projections showed that the incidence of PD was increasing continuously each year, with a wider age range as well. A large number of studies indicated that voltage-gated potassium channel (Kv) played significant roles in cellular signaling in both excitable and non-excitable cells. What’s more, Kv was also ubiquitously expressed in neurons and participated in signaling pathway in neurons. Kv1.5 (encoded by KCNA5) is an important voltage-gated K+ channel, which is not only necessary for critical processes such as cell proliferation and apoptosis but ubiquitously expressed in neurons. Recent studies reported that PD clinical drugs could inhibit the expression of Kv1.5. To determine the mechanisms by which Kv1.5 protects against MPP+ mediated neurotoxicity in PC12 cells. Materials and Methods: Knockdown of Kv1.5 model was established with pSINsi-hU6- Kv1.5 treated by the RNAi method in PC12. MTT, and Western Blot were used to detect the influence of Kv1.5 on PC12 proliferation, and the effect of Kv1.5 on PC12 apoptosis after MPP+ treatment in vitro. Results: 1) Knockdown and overexpression of Kv1.5 participated in PC12 proliferation. Transiently over-expressed Kv1.5 could boost the survival rate of PC12, while transiently knockdown of Kv1.5 inhibited PC12 proliferation. 2) The effect of Kv1.5 on PC12 proliferation was through PI3K/Akt signaling pathway. Over-expressed Kv1.5 could induce the activation of Akt, and Bcl-2 expression in PC12; Knockdown of Kv1.5 in PC12 inhibited the activation of Akt, Bcl-2 expression, and promoted MAPK phosphorylation. 3) Over-expressed Kv1.5 could significantly prevent PC12 from apoptosis induced by MPP+ via activating Akt pathway and increasing Bcl-2 expression; Knockdown of Kv1.5 was more sensitive than its control counterpart when treated with MPP+ for 24 h. Conclusion: Kv1.5 could hinder MPP+ neurotoxicity to PC12 by PI3K/Akt signaling pathway.},
 year = {2014}
}

Copy | Download

TY  - JOUR
T1  - Voltage-Gated Potassium Channel KV1.5 Protects against MPP+ Mediated Neurotoxicity in PC12 Cells
AU  - Chao Qu
AU  - Xiao-Zhen Fu
AU  - Chao Han
AU  - Qian Chen
AU  - Yan Liu
AU  - Xiao-bo Wang
AU  - Rong-Gang Xi
AU  - Jing Liu
AU  - Wei Zou
Y1  - 2014/12/31
PY  - 2014
N1  - https://doi.org/10.11648/j.ab.20140206.14
DO  - 10.11648/j.ab.20140206.14
T2  - Advances in Biochemistry
JF  - Advances in Biochemistry
JO  - Advances in Biochemistry
SP  - 103
EP  - 108
PB  - Science Publishing Group
SN  - 2329-0862
UR  - https://doi.org/10.11648/j.ab.20140206.14
AB  - Background: Parkinson’s disease (PD) is the second most common neurodegenerative disease and afflicts almost 1.8% of over 65-year-old group in the world. Epidemiological projections showed that the incidence of PD was increasing continuously each year, with a wider age range as well. A large number of studies indicated that voltage-gated potassium channel (Kv) played significant roles in cellular signaling in both excitable and non-excitable cells. What’s more, Kv was also ubiquitously expressed in neurons and participated in signaling pathway in neurons. Kv1.5 (encoded by KCNA5) is an important voltage-gated K+ channel, which is not only necessary for critical processes such as cell proliferation and apoptosis but ubiquitously expressed in neurons. Recent studies reported that PD clinical drugs could inhibit the expression of Kv1.5. To determine the mechanisms by which Kv1.5 protects against MPP+ mediated neurotoxicity in PC12 cells. Materials and Methods: Knockdown of Kv1.5 model was established with pSINsi-hU6- Kv1.5 treated by the RNAi method in PC12. MTT, and Western Blot were used to detect the influence of Kv1.5 on PC12 proliferation, and the effect of Kv1.5 on PC12 apoptosis after MPP+ treatment in vitro. Results: 1) Knockdown and overexpression of Kv1.5 participated in PC12 proliferation. Transiently over-expressed Kv1.5 could boost the survival rate of PC12, while transiently knockdown of Kv1.5 inhibited PC12 proliferation. 2) The effect of Kv1.5 on PC12 proliferation was through PI3K/Akt signaling pathway. Over-expressed Kv1.5 could induce the activation of Akt, and Bcl-2 expression in PC12; Knockdown of Kv1.5 in PC12 inhibited the activation of Akt, Bcl-2 expression, and promoted MAPK phosphorylation. 3) Over-expressed Kv1.5 could significantly prevent PC12 from apoptosis induced by MPP+ via activating Akt pathway and increasing Bcl-2 expression; Knockdown of Kv1.5 was more sensitive than its control counterpart when treated with MPP+ for 24 h. Conclusion: Kv1.5 could hinder MPP+ neurotoxicity to PC12 by PI3K/Akt signaling pathway.
VL  - 2
IS  - 6
ER  -

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