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Regulation of [Ca(2+)](i) oscillations and mitochondrial activity by various calcium transporters in mouse oocytes

Oocyte activation inefficiency is one of the reasons for female infertility and Ca(2+) functions play a critical role in the regulation of oocyte activation. We used various inhibitors of Ca(2+) channels located on the membrane, including sarcoplasmic/ endoplasmic reticulum Ca(2+)ATPases (SERCAs, th...

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Autores principales: Wang, Feng, Li, Ang, Meng, Tie-Gang, Wang, Le-Yun, Wang, Li-Juan, Hou, Yi, Schatten, Heide, Sun, Qing-Yuan, Ou, Xiang-Hong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7429721/
https://www.ncbi.nlm.nih.gov/pubmed/32799904
http://dx.doi.org/10.1186/s12958-020-00643-7
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author Wang, Feng
Li, Ang
Meng, Tie-Gang
Wang, Le-Yun
Wang, Li-Juan
Hou, Yi
Schatten, Heide
Sun, Qing-Yuan
Ou, Xiang-Hong
author_facet Wang, Feng
Li, Ang
Meng, Tie-Gang
Wang, Le-Yun
Wang, Li-Juan
Hou, Yi
Schatten, Heide
Sun, Qing-Yuan
Ou, Xiang-Hong
author_sort Wang, Feng
collection PubMed
description Oocyte activation inefficiency is one of the reasons for female infertility and Ca(2+) functions play a critical role in the regulation of oocyte activation. We used various inhibitors of Ca(2+) channels located on the membrane, including sarcoplasmic/ endoplasmic reticulum Ca(2+)ATPases (SERCAs, the main Ca(2+) pumps which decrease the intracellular Ca(2+) level by refilling Ca(2+) into the sarcoplasmic reticulum), transient receptor potential (TRP) ion channel subfamily member 7 (TRPM7, a Ca(2+)/Mg(2+)-permeable non-selective cation channel), T-type Ca(2+) channels and calcium channel Orai1, to investigate their roles in [Ca(2+)](i) oscillation patterns and mitochondrial membrane potential during oocyte activation by real-time recording. Our results showed that SERCAs, TRPM7 and T-type Ca(2+) channels were important for initiation and maintenance of [Ca(2+)](i) oscillations, which was required for mitochondrial membrane potential elevation during oocyte activation, as well as oocyte cytoskeleton stability and subsequent embryo development. Increasing the knowledge of calcium transport may provide a theoretical basis for improving oocyte activation in human assisted reproduction clinics.
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spelling pubmed-74297212020-08-18 Regulation of [Ca(2+)](i) oscillations and mitochondrial activity by various calcium transporters in mouse oocytes Wang, Feng Li, Ang Meng, Tie-Gang Wang, Le-Yun Wang, Li-Juan Hou, Yi Schatten, Heide Sun, Qing-Yuan Ou, Xiang-Hong Reprod Biol Endocrinol Research Oocyte activation inefficiency is one of the reasons for female infertility and Ca(2+) functions play a critical role in the regulation of oocyte activation. We used various inhibitors of Ca(2+) channels located on the membrane, including sarcoplasmic/ endoplasmic reticulum Ca(2+)ATPases (SERCAs, the main Ca(2+) pumps which decrease the intracellular Ca(2+) level by refilling Ca(2+) into the sarcoplasmic reticulum), transient receptor potential (TRP) ion channel subfamily member 7 (TRPM7, a Ca(2+)/Mg(2+)-permeable non-selective cation channel), T-type Ca(2+) channels and calcium channel Orai1, to investigate their roles in [Ca(2+)](i) oscillation patterns and mitochondrial membrane potential during oocyte activation by real-time recording. Our results showed that SERCAs, TRPM7 and T-type Ca(2+) channels were important for initiation and maintenance of [Ca(2+)](i) oscillations, which was required for mitochondrial membrane potential elevation during oocyte activation, as well as oocyte cytoskeleton stability and subsequent embryo development. Increasing the knowledge of calcium transport may provide a theoretical basis for improving oocyte activation in human assisted reproduction clinics. BioMed Central 2020-08-15 /pmc/articles/PMC7429721/ /pubmed/32799904 http://dx.doi.org/10.1186/s12958-020-00643-7 Text en © The Author(s) 2020 Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research
Wang, Feng
Li, Ang
Meng, Tie-Gang
Wang, Le-Yun
Wang, Li-Juan
Hou, Yi
Schatten, Heide
Sun, Qing-Yuan
Ou, Xiang-Hong
Regulation of [Ca(2+)](i) oscillations and mitochondrial activity by various calcium transporters in mouse oocytes
title Regulation of [Ca(2+)](i) oscillations and mitochondrial activity by various calcium transporters in mouse oocytes
title_full Regulation of [Ca(2+)](i) oscillations and mitochondrial activity by various calcium transporters in mouse oocytes
title_fullStr Regulation of [Ca(2+)](i) oscillations and mitochondrial activity by various calcium transporters in mouse oocytes
title_full_unstemmed Regulation of [Ca(2+)](i) oscillations and mitochondrial activity by various calcium transporters in mouse oocytes
title_short Regulation of [Ca(2+)](i) oscillations and mitochondrial activity by various calcium transporters in mouse oocytes
title_sort regulation of [ca(2+)](i) oscillations and mitochondrial activity by various calcium transporters in mouse oocytes
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7429721/
https://www.ncbi.nlm.nih.gov/pubmed/32799904
http://dx.doi.org/10.1186/s12958-020-00643-7
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