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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...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2020
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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 |
Sumario: | 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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