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The Role of Ca(2 +) in Maturation and Reprogramming of Bovine Oocytes: A System Study of Low-Calcium Model

[Ca(2+)](i) is essential for mammalian oocyte maturation and early embryonic development, as those processes are Ca(2+) dependent. In the present study, we investigated the effect of [Ca(2+)](i) on in vitro maturation and reprogramming of oocytes in a lower calcium model of oocyte at metaphase II (M...

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Autores principales: Meng, Lin, Hu, Hongmei, Liu, Zhiqiang, Zhang, Luyao, Zhuan, Qingrui, Li, Xue, Fu, Xiangwei, Zhu, Shien, Hou, Yunpeng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8577575/
https://www.ncbi.nlm.nih.gov/pubmed/34765601
http://dx.doi.org/10.3389/fcell.2021.746237
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author Meng, Lin
Hu, Hongmei
Liu, Zhiqiang
Zhang, Luyao
Zhuan, Qingrui
Li, Xue
Fu, Xiangwei
Zhu, Shien
Hou, Yunpeng
author_facet Meng, Lin
Hu, Hongmei
Liu, Zhiqiang
Zhang, Luyao
Zhuan, Qingrui
Li, Xue
Fu, Xiangwei
Zhu, Shien
Hou, Yunpeng
author_sort Meng, Lin
collection PubMed
description [Ca(2+)](i) is essential for mammalian oocyte maturation and early embryonic development, as those processes are Ca(2+) dependent. In the present study, we investigated the effect of [Ca(2+)](i) on in vitro maturation and reprogramming of oocytes in a lower calcium model of oocyte at metaphase II (MII) stage, which was established by adding cell-permeant Ca(2+) chelator BAPTA-AM to the maturation medium. Results showed that the extrusion of the first polar body (PB1) was delayed, and oocyte cytoplasmic maturation, including mitochondrial and endoplasmic reticulum distribution, was impaired in lower calcium model. The low-calcium-model oocytes presented a poor developmental phenotype of somatic cell nuclear transfer (SCNT) embryos at the beginning of activation of zygotic genome. At the same time, oxidative stress and apoptosis were observed in the low-calcium-model oocytes; subsequently, an RNA-seq analysis of the lower-calcium-model oocytes screened 24 genes responsible for the poor oocyte reprogramming, and six genes (ID1, SOX2, DPPA3, ASF1A, MSL3, and KDM6B) were identified by quantitative PCR. Analyzing the expression of these genes is helpful to elucidate the mechanisms of [Ca(2+)](i) regulating oocyte reprogramming. The most significant difference gene in this enriched item was ID1. Our results showed that the low calcium might give rise to oxidative stress and apoptosis, resulting in impaired maturation of bovine oocytes and possibly affecting subsequent reprogramming ability through the reduction of ID1.
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spelling pubmed-85775752021-11-10 The Role of Ca(2 +) in Maturation and Reprogramming of Bovine Oocytes: A System Study of Low-Calcium Model Meng, Lin Hu, Hongmei Liu, Zhiqiang Zhang, Luyao Zhuan, Qingrui Li, Xue Fu, Xiangwei Zhu, Shien Hou, Yunpeng Front Cell Dev Biol Cell and Developmental Biology [Ca(2+)](i) is essential for mammalian oocyte maturation and early embryonic development, as those processes are Ca(2+) dependent. In the present study, we investigated the effect of [Ca(2+)](i) on in vitro maturation and reprogramming of oocytes in a lower calcium model of oocyte at metaphase II (MII) stage, which was established by adding cell-permeant Ca(2+) chelator BAPTA-AM to the maturation medium. Results showed that the extrusion of the first polar body (PB1) was delayed, and oocyte cytoplasmic maturation, including mitochondrial and endoplasmic reticulum distribution, was impaired in lower calcium model. The low-calcium-model oocytes presented a poor developmental phenotype of somatic cell nuclear transfer (SCNT) embryos at the beginning of activation of zygotic genome. At the same time, oxidative stress and apoptosis were observed in the low-calcium-model oocytes; subsequently, an RNA-seq analysis of the lower-calcium-model oocytes screened 24 genes responsible for the poor oocyte reprogramming, and six genes (ID1, SOX2, DPPA3, ASF1A, MSL3, and KDM6B) were identified by quantitative PCR. Analyzing the expression of these genes is helpful to elucidate the mechanisms of [Ca(2+)](i) regulating oocyte reprogramming. The most significant difference gene in this enriched item was ID1. Our results showed that the low calcium might give rise to oxidative stress and apoptosis, resulting in impaired maturation of bovine oocytes and possibly affecting subsequent reprogramming ability through the reduction of ID1. Frontiers Media S.A. 2021-10-26 /pmc/articles/PMC8577575/ /pubmed/34765601 http://dx.doi.org/10.3389/fcell.2021.746237 Text en Copyright © 2021 Meng, Hu, Liu, Zhang, Zhuan, Li, Fu, Zhu and Hou. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Cell and Developmental Biology
Meng, Lin
Hu, Hongmei
Liu, Zhiqiang
Zhang, Luyao
Zhuan, Qingrui
Li, Xue
Fu, Xiangwei
Zhu, Shien
Hou, Yunpeng
The Role of Ca(2 +) in Maturation and Reprogramming of Bovine Oocytes: A System Study of Low-Calcium Model
title The Role of Ca(2 +) in Maturation and Reprogramming of Bovine Oocytes: A System Study of Low-Calcium Model
title_full The Role of Ca(2 +) in Maturation and Reprogramming of Bovine Oocytes: A System Study of Low-Calcium Model
title_fullStr The Role of Ca(2 +) in Maturation and Reprogramming of Bovine Oocytes: A System Study of Low-Calcium Model
title_full_unstemmed The Role of Ca(2 +) in Maturation and Reprogramming of Bovine Oocytes: A System Study of Low-Calcium Model
title_short The Role of Ca(2 +) in Maturation and Reprogramming of Bovine Oocytes: A System Study of Low-Calcium Model
title_sort role of ca(2 +) in maturation and reprogramming of bovine oocytes: a system study of low-calcium model
topic Cell and Developmental Biology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8577575/
https://www.ncbi.nlm.nih.gov/pubmed/34765601
http://dx.doi.org/10.3389/fcell.2021.746237
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