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TRPM7-like channels are functionally expressed in oocytes and modulate post-fertilization embryo development in mouse
The Transient Receptor Potential (TRP) channels are a family of cationic ion channels widely distributed in mammalian tissues. In general, the global genetic disruption of individual TRP channels result in phenotypes associated with impairment of a particular tissue and/or organ function. An excepti...
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/PMC5041074/ https://www.ncbi.nlm.nih.gov/pubmed/27681336 http://dx.doi.org/10.1038/srep34236 |
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author | Carvacho, Ingrid Ardestani, Goli Lee, Hoi Chang McGarvey, Kaitlyn Fissore, Rafael A. Lykke-Hartmann, Karin |
author_facet | Carvacho, Ingrid Ardestani, Goli Lee, Hoi Chang McGarvey, Kaitlyn Fissore, Rafael A. Lykke-Hartmann, Karin |
author_sort | Carvacho, Ingrid |
collection | PubMed |
description | The Transient Receptor Potential (TRP) channels are a family of cationic ion channels widely distributed in mammalian tissues. In general, the global genetic disruption of individual TRP channels result in phenotypes associated with impairment of a particular tissue and/or organ function. An exception is the genetic ablation of the TRP channel TRPM7, which results in early embryonic lethality. Nevertheless, the function of TRPM7 in oocytes, eggs and pre-implantation embryos remains unknown. Here, we described an outward rectifying non-selective current mediated by a TRP ion channel in immature oocytes (germinal vesicle stage), matured oocytes (metaphase II eggs) and 2-cell stage embryos. The current is activated by specific agonists and inhibited by distinct blockers consistent with the functional expression of TRPM7 channels. We demonstrated that the TRPM7-like channels are homo-tetramers and their activation mediates calcium influx in oocytes and eggs, which is fundamental to support fertilization and egg activation. Lastly, we showed that pharmacological inhibition of the channel function delays pre-implantation embryo development and reduces progression to the blastocyst stage. Our data demonstrate functional expression of TRPM7-like channels in mouse oocytes, eggs and embryos that may play an essential role in the initiation of embryo development. |
format | Online Article Text |
id | pubmed-5041074 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-50410742016-09-30 TRPM7-like channels are functionally expressed in oocytes and modulate post-fertilization embryo development in mouse Carvacho, Ingrid Ardestani, Goli Lee, Hoi Chang McGarvey, Kaitlyn Fissore, Rafael A. Lykke-Hartmann, Karin Sci Rep Article The Transient Receptor Potential (TRP) channels are a family of cationic ion channels widely distributed in mammalian tissues. In general, the global genetic disruption of individual TRP channels result in phenotypes associated with impairment of a particular tissue and/or organ function. An exception is the genetic ablation of the TRP channel TRPM7, which results in early embryonic lethality. Nevertheless, the function of TRPM7 in oocytes, eggs and pre-implantation embryos remains unknown. Here, we described an outward rectifying non-selective current mediated by a TRP ion channel in immature oocytes (germinal vesicle stage), matured oocytes (metaphase II eggs) and 2-cell stage embryos. The current is activated by specific agonists and inhibited by distinct blockers consistent with the functional expression of TRPM7 channels. We demonstrated that the TRPM7-like channels are homo-tetramers and their activation mediates calcium influx in oocytes and eggs, which is fundamental to support fertilization and egg activation. Lastly, we showed that pharmacological inhibition of the channel function delays pre-implantation embryo development and reduces progression to the blastocyst stage. Our data demonstrate functional expression of TRPM7-like channels in mouse oocytes, eggs and embryos that may play an essential role in the initiation of embryo development. Nature Publishing Group 2016-09-29 /pmc/articles/PMC5041074/ /pubmed/27681336 http://dx.doi.org/10.1038/srep34236 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 Carvacho, Ingrid Ardestani, Goli Lee, Hoi Chang McGarvey, Kaitlyn Fissore, Rafael A. Lykke-Hartmann, Karin TRPM7-like channels are functionally expressed in oocytes and modulate post-fertilization embryo development in mouse |
title | TRPM7-like channels are functionally expressed in oocytes and modulate post-fertilization embryo development in mouse |
title_full | TRPM7-like channels are functionally expressed in oocytes and modulate post-fertilization embryo development in mouse |
title_fullStr | TRPM7-like channels are functionally expressed in oocytes and modulate post-fertilization embryo development in mouse |
title_full_unstemmed | TRPM7-like channels are functionally expressed in oocytes and modulate post-fertilization embryo development in mouse |
title_short | TRPM7-like channels are functionally expressed in oocytes and modulate post-fertilization embryo development in mouse |
title_sort | trpm7-like channels are functionally expressed in oocytes and modulate post-fertilization embryo development in mouse |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5041074/ https://www.ncbi.nlm.nih.gov/pubmed/27681336 http://dx.doi.org/10.1038/srep34236 |
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