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Distinct mechanisms regulating mechanical force-induced Ca(2+) signals at the plasma membrane and the ER in human MSCs
It is unclear that how subcellular organelles respond to external mechanical stimuli. Here, we investigated the molecular mechanisms by which mechanical force regulates Ca(2+) signaling at endoplasmic reticulum (ER) in human mesenchymal stem cells. Without extracellular Ca(2+), ER Ca(2+) release is...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
eLife Sciences Publications, Ltd
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4337650/ https://www.ncbi.nlm.nih.gov/pubmed/25667984 http://dx.doi.org/10.7554/eLife.04876 |
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author | Kim, Tae-Jin Joo, Chirlmin Seong, Jihye Vafabakhsh, Reza Botvinick, Elliot L Berns, Michael W Palmer, Amy E Wang, Ning Ha, Taekjip Jakobsson, Eric Sun, Jie Wang, Yingxiao |
author_facet | Kim, Tae-Jin Joo, Chirlmin Seong, Jihye Vafabakhsh, Reza Botvinick, Elliot L Berns, Michael W Palmer, Amy E Wang, Ning Ha, Taekjip Jakobsson, Eric Sun, Jie Wang, Yingxiao |
author_sort | Kim, Tae-Jin |
collection | PubMed |
description | It is unclear that how subcellular organelles respond to external mechanical stimuli. Here, we investigated the molecular mechanisms by which mechanical force regulates Ca(2+) signaling at endoplasmic reticulum (ER) in human mesenchymal stem cells. Without extracellular Ca(2+), ER Ca(2+) release is the source of intracellular Ca(2+) oscillations induced by laser-tweezer-traction at the plasma membrane, providing a model to study how mechanical stimuli can be transmitted deep inside the cell body. This ER Ca(2+) release upon mechanical stimulation is mediated not only by the mechanical support of cytoskeleton and actomyosin contractility, but also by mechanosensitive Ca(2+) permeable channels on the plasma membrane, specifically TRPM7. However, Ca(2+) influx at the plasma membrane via mechanosensitive Ca(2+) permeable channels is only mediated by the passive cytoskeletal structure but not active actomyosin contractility. Thus, active actomyosin contractility is essential for the response of ER to the external mechanical stimuli, distinct from the mechanical regulation at the plasma membrane. DOI: http://dx.doi.org/10.7554/eLife.04876.001 |
format | Online Article Text |
id | pubmed-4337650 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | eLife Sciences Publications, Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-43376502015-03-04 Distinct mechanisms regulating mechanical force-induced Ca(2+) signals at the plasma membrane and the ER in human MSCs Kim, Tae-Jin Joo, Chirlmin Seong, Jihye Vafabakhsh, Reza Botvinick, Elliot L Berns, Michael W Palmer, Amy E Wang, Ning Ha, Taekjip Jakobsson, Eric Sun, Jie Wang, Yingxiao eLife Biophysics and Structural Biology It is unclear that how subcellular organelles respond to external mechanical stimuli. Here, we investigated the molecular mechanisms by which mechanical force regulates Ca(2+) signaling at endoplasmic reticulum (ER) in human mesenchymal stem cells. Without extracellular Ca(2+), ER Ca(2+) release is the source of intracellular Ca(2+) oscillations induced by laser-tweezer-traction at the plasma membrane, providing a model to study how mechanical stimuli can be transmitted deep inside the cell body. This ER Ca(2+) release upon mechanical stimulation is mediated not only by the mechanical support of cytoskeleton and actomyosin contractility, but also by mechanosensitive Ca(2+) permeable channels on the plasma membrane, specifically TRPM7. However, Ca(2+) influx at the plasma membrane via mechanosensitive Ca(2+) permeable channels is only mediated by the passive cytoskeletal structure but not active actomyosin contractility. Thus, active actomyosin contractility is essential for the response of ER to the external mechanical stimuli, distinct from the mechanical regulation at the plasma membrane. DOI: http://dx.doi.org/10.7554/eLife.04876.001 eLife Sciences Publications, Ltd 2015-02-10 /pmc/articles/PMC4337650/ /pubmed/25667984 http://dx.doi.org/10.7554/eLife.04876 Text en © 2015, Kim et al http://creativecommons.org/licenses/by/4.0/ This article is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use and redistribution provided that the original author and source are credited. |
spellingShingle | Biophysics and Structural Biology Kim, Tae-Jin Joo, Chirlmin Seong, Jihye Vafabakhsh, Reza Botvinick, Elliot L Berns, Michael W Palmer, Amy E Wang, Ning Ha, Taekjip Jakobsson, Eric Sun, Jie Wang, Yingxiao Distinct mechanisms regulating mechanical force-induced Ca(2+) signals at the plasma membrane and the ER in human MSCs |
title | Distinct mechanisms regulating mechanical force-induced Ca(2+) signals at the plasma membrane and the ER in human MSCs |
title_full | Distinct mechanisms regulating mechanical force-induced Ca(2+) signals at the plasma membrane and the ER in human MSCs |
title_fullStr | Distinct mechanisms regulating mechanical force-induced Ca(2+) signals at the plasma membrane and the ER in human MSCs |
title_full_unstemmed | Distinct mechanisms regulating mechanical force-induced Ca(2+) signals at the plasma membrane and the ER in human MSCs |
title_short | Distinct mechanisms regulating mechanical force-induced Ca(2+) signals at the plasma membrane and the ER in human MSCs |
title_sort | distinct mechanisms regulating mechanical force-induced ca(2+) signals at the plasma membrane and the er in human mscs |
topic | Biophysics and Structural Biology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4337650/ https://www.ncbi.nlm.nih.gov/pubmed/25667984 http://dx.doi.org/10.7554/eLife.04876 |
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