Reactive oxygen species-mediated unfolded protein response pathways in preimplantation embryos

Ali, Ihsan; Shah, Syed Zahid Ali; Jin, Yi; Li, Zhongshu; Ullah, Obaid; Nan-zhu, Fang

doi:10.4142/jvs.2017.18.1.1

Cited by 14 publications

(8 citation statements)

References 101 publications

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“…The major obstacles in in vitro embryo development are the production of excessive free radicals and exposure to oxidative stress. When ROS production exceeds the antioxidant capacity of embryos, oxidative stress occurs 24 , 25 . The production of ROS is particular critical in early embryonic development, and excessive ROS will induce apoptosis and metabolic disorders 26 , 27 .…”

Section: Discussionmentioning

confidence: 99%

The possible molecular mechanisms of bisphenol A action on porcine early embryonic development

Guo

Zhao

Shin

et al. 2017

Sci Rep

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Bisphenol A (BPA) is an environmental contaminant widely used in the plastic industry. BPA has been demonstrated to be an endocrine disruptor and has an adverse effect on the embryonic development of mammals. However, the mechanism of action of BPA is limited. In this study, we investigated the role and mechanism of BPA in porcine embryonic development. First, the parthenotes were treated with different concentrations of BPA. We found that blastocyst formation was impaired and the parthenotes were arrested at the 4-cell stage after treatment with 100 μm BPA. Second, ROS increased following the addition of BPA, which further caused mitochondrial damage, and cytochrome c was released from the mitochondria to induce apoptosis. The adaptive response was demonstrated through LC3 immunofluorescence staining and by assessing autophagy-related gene expression. In addition, BPA caused DNA damage through the p53-p21 signaling pathway. Thus, our results indicate that BPA displays an adverse effect on porcine early embryonic development through mitochondrial and DNA damage.

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Section: Discussionmentioning

confidence: 99%

The possible molecular mechanisms of bisphenol A action on porcine early embryonic development

Guo

Zhao

Shin

et al. 2017

Sci Rep

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“…It is a major site for the synthesis of transmembrane proteins and lipids, and is involved in maintaining intracellular calcium homeostasis [1,2,17]. The ER quality control (ERQC) system is in charge of identifying properly folded proteins, which are channeled for transport to the Golgi complex, versus misfolded proteins, which are retained in the ER to undergo correct folding or be targeted for degradation by the ER-associated degradation (ERAD) machinery [18]. Correct protein folding is one of the most important steps during protein synthesis, and the accumulation of misfolded proteins in the ER lumen disturbs ER functions and leads to ER stress.…”

Section: Endoplasmic Reticulum Stress and Unfolded Protein Responsmentioning

confidence: 99%

“…The PERK-mediated phosphorylation of eIF2α at ser51 initiates translation [20]. Phosphorylated eIF2α binds the guanine nucleotide exchange factor, eIF2B, to interfere with the cell’s ability to exchange guanosine diphosphate (GDP) with guanosine triphosphate (GTP) to form eIF2-GTP tRNA [18,21]. Thus, phosphorylation of eIF2α is thought to be an important step in reducing the synthesis of new proteins in the ER, releasing ER stress and restoring ER homeostasis [5,21].…”

Section: Endoplasmic Reticulum Stress and Unfolded Protein Responsmentioning

confidence: 99%

Endoplasmic Reticulum (ER) Stress and Unfolded Protein Response (UPR) in Mammalian Oocyte Maturation and Preimplantation Embryo Development

Lin

Lee

Kang

et al. 2019

IJMS

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Mammalian oocytes and early embryos derived from in vitro production are highly susceptible to a variety of cellular stresses. During oocyte maturation and preimplantation embryo development, functional proteins must be folded properly in the endoplasmic reticulum (ER) to maintain oocyte and embryo development. However, some adverse factors negatively impact ER functions and protein synthesis, resulting in the activation of ER stress and unfolded protein response (UPR) signaling pathways. ER stress and UPR signaling have been identified in mammalian oocytes and embryos produced in vitro, suggesting that modulation of ER stress and UPR signaling play very important roles in oocyte maturation and the development of preimplantation embryos. In this review, we briefly describe the current state of knowledge regarding ER stress, UPR signaling pathways, and their roles and mechanisms in mammalian (excluding human) oocyte maturation and preimplantation embryo development.

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“…These processes are known to affect the early development of porcine embryos. Particularly, ROS generated from diverse sources can cause oxidative damage to embryos and thus impair embryonic development (Guerin et al, 2001; Ali et al, 2017). Such an oxidative stress further disrupts mitochondrial potential, which decreases ATP generation.…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2020

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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.

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Reactive oxygen species-mediated unfolded protein response pathways in preimplantation embryos

Cited by 14 publications

References 101 publications

The possible molecular mechanisms of bisphenol A action on porcine early embryonic development

The possible molecular mechanisms of bisphenol A action on porcine early embryonic development

Endoplasmic Reticulum (ER) Stress and Unfolded Protein Response (UPR) in Mammalian Oocyte Maturation and Preimplantation Embryo Development

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

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