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The Role of Kv1.2 Channel in Electrotaxis Cell Migration
Voltage‐gated potassium Kv1.2 channels play pivotal role in maintaining of resting membrane potential and, consequently, regulation of cellular excitability of neurons. Endogenously generated electric field (EF) have been proven as an important regulator for cell migration and tissue repair. The mec...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4832312/ https://www.ncbi.nlm.nih.gov/pubmed/26580832 http://dx.doi.org/10.1002/jcp.25259 |
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author | Zhang, Gaofeng Edmundson, Mathew Telezhkin, Vsevolod Gu, Yu Wei, Xiaoqing Kemp, Paul J. Song, Bing |
author_facet | Zhang, Gaofeng Edmundson, Mathew Telezhkin, Vsevolod Gu, Yu Wei, Xiaoqing Kemp, Paul J. Song, Bing |
author_sort | Zhang, Gaofeng |
collection | PubMed |
description | Voltage‐gated potassium Kv1.2 channels play pivotal role in maintaining of resting membrane potential and, consequently, regulation of cellular excitability of neurons. Endogenously generated electric field (EF) have been proven as an important regulator for cell migration and tissue repair. The mechanisms of ion channel involvement in EF‐induced cell responses are extensively studied but largely are poorly understood. In this study we generated three COS‐7 clones with different expression levels of Kv1.2 channel, and confirmed their functional variations with patch clamp analysis. Time‐lapse imaging analysis showed that EF‐induced cell migration response was Kv1.2 channel expression level depended. Inhibition of Kv1.2 channels with charybdotoxin (ChTX) constrained the sensitivity of COS‐7 cells to EF stimulation more than their motility. Immunocytochemistry and pull‐down analyses demonstrated association of Kv1.2 channels with actin‐binding protein cortactin and its re‐localization to the cathode‐facing membrane at EF stimulation, which confirms the mechanism of EF‐induced directional migration. This study displays that Kv1.2 channels represent an important physiological link in EF‐induced cell migration. The described mechanism suggests a potential application of EF which may improve therapeutic performance in curing injuries of neuronal and/or cardiac tissue repair, post operational therapy, and various degenerative syndromes. J. Cell. Physiol. 231: 1375–1384, 2016. © 2015 The Authors. Journal of Cellular Physiology Published by Wiley Periodicals, Inc. |
format | Online Article Text |
id | pubmed-4832312 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-48323122016-04-20 The Role of Kv1.2 Channel in Electrotaxis Cell Migration Zhang, Gaofeng Edmundson, Mathew Telezhkin, Vsevolod Gu, Yu Wei, Xiaoqing Kemp, Paul J. Song, Bing J Cell Physiol Original Research Articles Voltage‐gated potassium Kv1.2 channels play pivotal role in maintaining of resting membrane potential and, consequently, regulation of cellular excitability of neurons. Endogenously generated electric field (EF) have been proven as an important regulator for cell migration and tissue repair. The mechanisms of ion channel involvement in EF‐induced cell responses are extensively studied but largely are poorly understood. In this study we generated three COS‐7 clones with different expression levels of Kv1.2 channel, and confirmed their functional variations with patch clamp analysis. Time‐lapse imaging analysis showed that EF‐induced cell migration response was Kv1.2 channel expression level depended. Inhibition of Kv1.2 channels with charybdotoxin (ChTX) constrained the sensitivity of COS‐7 cells to EF stimulation more than their motility. Immunocytochemistry and pull‐down analyses demonstrated association of Kv1.2 channels with actin‐binding protein cortactin and its re‐localization to the cathode‐facing membrane at EF stimulation, which confirms the mechanism of EF‐induced directional migration. This study displays that Kv1.2 channels represent an important physiological link in EF‐induced cell migration. The described mechanism suggests a potential application of EF which may improve therapeutic performance in curing injuries of neuronal and/or cardiac tissue repair, post operational therapy, and various degenerative syndromes. J. Cell. Physiol. 231: 1375–1384, 2016. © 2015 The Authors. Journal of Cellular Physiology Published by Wiley Periodicals, Inc. John Wiley and Sons Inc. 2015-12-10 2016-06 /pmc/articles/PMC4832312/ /pubmed/26580832 http://dx.doi.org/10.1002/jcp.25259 Text en © 2015 The Authors. Journal of Cellular Physiology Published by Wiley Periodicals, Inc. This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Research Articles Zhang, Gaofeng Edmundson, Mathew Telezhkin, Vsevolod Gu, Yu Wei, Xiaoqing Kemp, Paul J. Song, Bing The Role of Kv1.2 Channel in Electrotaxis Cell Migration |
title | The Role of Kv1.2 Channel in Electrotaxis Cell Migration |
title_full | The Role of Kv1.2 Channel in Electrotaxis Cell Migration |
title_fullStr | The Role of Kv1.2 Channel in Electrotaxis Cell Migration |
title_full_unstemmed | The Role of Kv1.2 Channel in Electrotaxis Cell Migration |
title_short | The Role of Kv1.2 Channel in Electrotaxis Cell Migration |
title_sort | role of kv1.2 channel in electrotaxis cell migration |
topic | Original Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4832312/ https://www.ncbi.nlm.nih.gov/pubmed/26580832 http://dx.doi.org/10.1002/jcp.25259 |
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