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Connexin 43 Knockdown Induces Mitochondrial Dysfunction and Affects Early Developmental Competence in Porcine Embryos

Published online by Cambridge University Press:  10 February 2020

Kyung-Tae Shin
Affiliation:
Department of Animal Sciences, Chungbuk National University, Chungbuk, Cheongju361-763, Republic of Korea
Zheng-Wen Nie
Affiliation:
Department of Animal Sciences, Chungbuk National University, Chungbuk, Cheongju361-763, Republic of Korea
Wenjun Zhou
Affiliation:
Department of Animal Sciences, Chungbuk National University, Chungbuk, Cheongju361-763, Republic of Korea
Dongjie Zhou
Affiliation:
Department of Animal Sciences, Chungbuk National University, Chungbuk, Cheongju361-763, Republic of Korea
Ju-Yeon Kim
Affiliation:
Department of Animal Sciences, Chungbuk National University, Chungbuk, Cheongju361-763, Republic of Korea
Sun A. Ock
Affiliation:
Animal Biotechnology Division, National Institute of Animal Science, Rural Development Administration, Jeonju55365, Republic of Korea
Ying-Jie Niu
Affiliation:
Department of Animal Sciences, Chungbuk National University, Chungbuk, Cheongju361-763, Republic of Korea
Xiang-Shun Cui*
Affiliation:
Department of Animal Sciences, Chungbuk National University, Chungbuk, Cheongju361-763, Republic of Korea
*
*Author for correspondence: Xiang-Shun Cui, E-mail: xscui@cbnu.ac.kr
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Abstract

Connexin 43 (CX43) is a component of gap junctions. The lack of functional CX43 induces oxidative stress, autophagy, and apoptosis in somatic cells. However, the role of CX43 in the early development of porcine embryos is still unknown. Thus, the aim of this study was to investigate the role of CX43, and its underlying molecular mechanisms, on the developmental competence of early porcine embryos. We performed CX43 knockdown by microinjecting dsRNA into parthenogenetically activated porcine parthenotes. The blastocyst development rate and the total number of cells in the blastocysts were significantly reduced by CX43 knockdown. Results from FITC-dextran assays showed that CX43 knockdown significantly increased membrane permeability. ZO-1 protein was obliterated in CX43 knockdown blastocysts. Mitochondrial membrane potential and ATP production were significantly reduced following CX43 knockdown. Reactive oxygen species (ROS) levels were significantly increased in the CX43 knockdown group compared to those in control embryos. Moreover, CX43 knockdown induced autophagy and apoptosis. Our findings indicate that CX43 is essential for the development and preimplantation of porcine embryos and maintains mitochondrial function, cell junction structure, and cell homeostasis by regulating membrane permeability, ROS generation, autophagy, and apoptosis in early embryos.

Type
Biological Applications
Copyright
Copyright © Microscopy Society of America 2020

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