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TRPM4-mediated control of FcεRI-evoked Ca(2+) elevation comprises enhanced plasmalemmal trafficking of TRPM4 channels in connective tissue type mast cells
TRPM4 proteins form Ca(2+)-activated non selective cation (CAN) channels that affect transmembrane Ca(2+)-influx by determining the membrane potential. Tight control of the intracellular Ca(2+) concentration is essential for mast cell responses. In this study, we analyzed the expression of TRPM4 in...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5021962/ https://www.ncbi.nlm.nih.gov/pubmed/27624684 http://dx.doi.org/10.1038/srep32981 |
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author | Rixecker, Torben Mathar, Ilka Medert, Rebekka Mannebach, Stefanie Pfeifer, Alexander Lipp, Peter Tsvilovskyy, Volodymyr Freichel, Marc |
author_facet | Rixecker, Torben Mathar, Ilka Medert, Rebekka Mannebach, Stefanie Pfeifer, Alexander Lipp, Peter Tsvilovskyy, Volodymyr Freichel, Marc |
author_sort | Rixecker, Torben |
collection | PubMed |
description | TRPM4 proteins form Ca(2+)-activated non selective cation (CAN) channels that affect transmembrane Ca(2+)-influx by determining the membrane potential. Tight control of the intracellular Ca(2+) concentration is essential for mast cell responses. In this study, we analyzed the expression of TRPM4 in peritoneal mast cells (PCMC) as a model for connective tissue type mast cells with respect to FcεRI-evoked calcium changes and the subcellular localization of fluorescently labeled TRPM4 using two viral transduction systems before and following antigen stimulation. Our results show that TRPM4 is expressed in PCMCs, is an essential constituent of the endogenous CAN channels in PCMCs and regulates antigen-evoked increases in intracellular calcium that are significantly enhanced in TRPM4-deficient PCMCs. Compared to PCMCs analyzed before antigen stimulation, the cells depict a substantially increased localization of TRPM4 proteins towards the plasma membrane after FcεRI stimulation. Thus, TRPM4 functions as a limiting factor for antigen evoked calcium rise in connective tissue type mast cells and concurrent translocation of TRPM4 into the plasma membrane is part of this mechanism. |
format | Online Article Text |
id | pubmed-5021962 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-50219622016-09-20 TRPM4-mediated control of FcεRI-evoked Ca(2+) elevation comprises enhanced plasmalemmal trafficking of TRPM4 channels in connective tissue type mast cells Rixecker, Torben Mathar, Ilka Medert, Rebekka Mannebach, Stefanie Pfeifer, Alexander Lipp, Peter Tsvilovskyy, Volodymyr Freichel, Marc Sci Rep Article TRPM4 proteins form Ca(2+)-activated non selective cation (CAN) channels that affect transmembrane Ca(2+)-influx by determining the membrane potential. Tight control of the intracellular Ca(2+) concentration is essential for mast cell responses. In this study, we analyzed the expression of TRPM4 in peritoneal mast cells (PCMC) as a model for connective tissue type mast cells with respect to FcεRI-evoked calcium changes and the subcellular localization of fluorescently labeled TRPM4 using two viral transduction systems before and following antigen stimulation. Our results show that TRPM4 is expressed in PCMCs, is an essential constituent of the endogenous CAN channels in PCMCs and regulates antigen-evoked increases in intracellular calcium that are significantly enhanced in TRPM4-deficient PCMCs. Compared to PCMCs analyzed before antigen stimulation, the cells depict a substantially increased localization of TRPM4 proteins towards the plasma membrane after FcεRI stimulation. Thus, TRPM4 functions as a limiting factor for antigen evoked calcium rise in connective tissue type mast cells and concurrent translocation of TRPM4 into the plasma membrane is part of this mechanism. Nature Publishing Group 2016-09-14 /pmc/articles/PMC5021962/ /pubmed/27624684 http://dx.doi.org/10.1038/srep32981 Text en Copyright © 2016, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Rixecker, Torben Mathar, Ilka Medert, Rebekka Mannebach, Stefanie Pfeifer, Alexander Lipp, Peter Tsvilovskyy, Volodymyr Freichel, Marc TRPM4-mediated control of FcεRI-evoked Ca(2+) elevation comprises enhanced plasmalemmal trafficking of TRPM4 channels in connective tissue type mast cells |
title | TRPM4-mediated control of FcεRI-evoked Ca(2+) elevation comprises enhanced plasmalemmal trafficking of TRPM4 channels in connective tissue type mast cells |
title_full | TRPM4-mediated control of FcεRI-evoked Ca(2+) elevation comprises enhanced plasmalemmal trafficking of TRPM4 channels in connective tissue type mast cells |
title_fullStr | TRPM4-mediated control of FcεRI-evoked Ca(2+) elevation comprises enhanced plasmalemmal trafficking of TRPM4 channels in connective tissue type mast cells |
title_full_unstemmed | TRPM4-mediated control of FcεRI-evoked Ca(2+) elevation comprises enhanced plasmalemmal trafficking of TRPM4 channels in connective tissue type mast cells |
title_short | TRPM4-mediated control of FcεRI-evoked Ca(2+) elevation comprises enhanced plasmalemmal trafficking of TRPM4 channels in connective tissue type mast cells |
title_sort | trpm4-mediated control of fcεri-evoked ca(2+) elevation comprises enhanced plasmalemmal trafficking of trpm4 channels in connective tissue type mast cells |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5021962/ https://www.ncbi.nlm.nih.gov/pubmed/27624684 http://dx.doi.org/10.1038/srep32981 |
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