The regulation of autophagy in porcine blastocysts: Regulation of PARylation-mediated autophagy via mammalian target of rapamycin complex 1 (mTORC1) signaling

Lee, Hye Ran; Kim, Duk Hyoun; Kim, Min Gyeong; Lee, Jun Sung; Hwang, Jeong Ho; Lee, Hoon Taek

doi:10.1016/j.bbrc.2016.03.148

Cited by 10 publications

(7 citation statements)

References 22 publications

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“…The effect of PARylation on autophagic degradation was subsequently found to be mediated by the mTOR pathway (Lee et al, 2016b). Specifically, PARylation, which activates AMPK and negatively regulates the mTOR pathway (Zhou et al, 2013;Chen et al, 2015), causes autophagy during the blastocyst formation process in porcine embryos by decreasing p70S6K accumulation and thus inhibiting the activity of mTORC1 (Lee et al, 2016b). In this way, PARylation Xie et al, 2018;Imamura et al, 2004;Lee et al, 2016a;Zhou et al, 2013;Chen et al, 2015 accurately regulates the embryo development through MAPK and mTOR pathways.…”

Section: Parylation Is a Novel Marker Of Oocyte And Embryo Qualitymentioning

confidence: 99%

“…During blastocyst formation, inhibition of PARylation selectively suppresses autophagic degradation of ubiquitinated proteins ( Lee et al, 2016a ). The effect of PARylation on autophagic degradation was subsequently found to be mediated by the mTOR pathway ( Lee et al, 2016b ). Specifically, PARylation, which activates AMPK and negatively regulates the mTOR pathway ( Zhou et al, 2013 ; Chen et al, 2015 ), causes autophagy during the blastocyst formation process in porcine embryos by decreasing p70S6K accumulation and thus inhibiting the activity of mTORC1 ( Lee et al, 2016b ).…”

Section: Parylation Is a Novel Marker Of Oocyte And Embryo Qualitymentioning

confidence: 99%

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Post-Translational Modifications in Oocyte Maturation and Embryo Development

Yang

2021

Front. Cell Dev. Biol.

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Mammalian oocyte maturation and embryo development are unique biological processes regulated by various modifications. Since de novo mRNA transcription is absent during oocyte meiosis, protein-level regulation, especially post-translational modification (PTM), is crucial. It is known that PTM plays key roles in diverse cellular events such as DNA damage response, chromosome condensation, and cytoskeletal organization during oocyte maturation and embryo development. However, most previous reviews on PTM in oocytes and embryos have only focused on studies of Xenopus laevis or Caenorhabditis elegans eggs. In this review, we will discuss the latest discoveries regarding PTM in mammalian oocytes maturation and embryo development, focusing on phosphorylation, ubiquitination, SUMOylation and Poly(ADP-ribosyl)ation (PARylation). Phosphorylation functions in chromosome condensation and spindle alignment by regulating histone H3, mitogen-activated protein kinases, and some other pathways during mammalian oocyte maturation. Ubiquitination is a three-step enzymatic cascade that facilitates the degradation of proteins, and numerous E3 ubiquitin ligases are involved in modifying substrates and thus regulating oocyte maturation, oocyte-sperm binding, and early embryo development. Through the reversible addition and removal of SUMO (small ubiquitin-related modifier) on lysine residues, SUMOylation affects the cell cycle and DNA damage response in oocytes. As an emerging PTM, PARlation has been shown to not only participate in DNA damage repair, but also mediate asymmetric division of oocyte meiosis. Each of these PTMs and external environments is versatile and contributes to distinct phases during oocyte maturation and embryo development.

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Section: Parylation Is a Novel Marker Of Oocyte And Embryo Qualitymentioning

confidence: 99%

Section: Parylation Is a Novel Marker Of Oocyte And Embryo Qualitymentioning

confidence: 99%

Post-Translational Modifications in Oocyte Maturation and Embryo Development

Yang

2021

Front. Cell Dev. Biol.

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“…Inhibition of miR-128 by curcumin pretreatment in monocytes from AD patients improves Aβ (1-42) degradation (Howell et al, 2013;Tiribuzi et al, 2014). Another study put stress on the contribution of curcumin to neuroprotection from hippocampal neuronal cell death with origin of status epilepticus by provoking the production of Beclin-1 and LC3 (autophagy proteins), as well as the inhibition of mixed lineage kinase domain-like protein and receptor interaction protein kinase 1 (necroptosis proteins; H. R. Lee et al, 2016). Youssef, Peiris, Kelley, and Grant (2013) in an attempt to examine the role of vitamin D and curcumin in treating gonorrhea, suggested that there may be a synergic interplay between these two compounds, culminating in the improvement of gonorrhea through the synthesis of cathelicidin followed by an autophagic response.…”

Section: Neurologic Involvementmentioning

confidence: 99%

Curcumin: A naturally occurring autophagy modulator

Shakeri

Cicero

Panahi

et al. 2018

Journal Cellular Physiology

185

118

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Autophagy is a self-degradative process that plays a pivotal role in several medical conditions associated with infection, cancer, neurodegeneration, aging, and metabolic disorders. Its interplay with cancer development and treatment resistance is complicated and paramount for drug design since an autophagic response can lead to tumor suppression by enhancing cellular integrity and tumorigenesis by improving tumor cell survival. In addition, autophagy denotes the cellular ability of adapting to stress though it may end up in apoptosis activation when cells are exposed to a very powerful stress. Induction of autophagy is a therapeutic option in cancer and many anticancer drugs have been developed to this aim. Curcumin as a hydrophobic polyphenol compound extracted from the known spice turmeric has different pharmacological effects in both in vitro and in vivo models. Many reports exist reporting that curcumin is capable of triggering autophagy in several cancer cells. In this review, we will focus on how curcumin can target autophagy in different cellular settings that may extend our understanding of new pharmacological agents to overcome relevant diseases. K E Y W O R D S autophagy, cell death, curcumin, molecular mechanisms

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“…It can act as not only a defense mechanism to prevent environmental damage to cells also induces cell death in eukaryotes. The regulation of autophagy is achieved through ubiquitin-like protein systems [19], mammalian target of rapamycin (mTOR) [20], acetylated protein systems [21], methylation [22], microRNA (miRNA) [23], and transcription factors [24]. Autophagy-related genes (ATGs) play the key role in this process [8].…”

Section: Discussionmentioning

confidence: 99%

“…Autophagy-related genes (ATGs) play the key role in this process [8]. For example, autophagy can be induced by PI3K core complex which contains Beclin1/BECN1 (ATG6), ATG9, TAG14L, Ultraviolet Radiation Resistance-associated Gene Protein (UVRAG) and other proteins [25]. The extension of autophagosome membrane involves two ubiquitin-like proteins (ATG12 and ATG8/LC3).…”

Section: Discussionmentioning

confidence: 99%

Characteristics of Autophagy Induced by Enterovirus71 (EV71) Viral Protein

Li¹,

Jinxue²,

Liu³

et al. 2018

J Trop Dis

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Hand, Foot and Mouth Disease (HFMD) is a type of infectious disease that is more commonly seen in children under the age of 6 years. It was first reported in New Zealand in 1957, and then outbreaks occurred in Europe, America and Asia. In recent years, the incidence of HFMD in China is also on the rise. HFMD was caused by Coxsackievirus A16 (CVA16) and Human Enterovirus 71 (EV71) and other virus. CVA16 usually causes mild cases and is less harmful, while EV71 infection causes not only mild cases, but also severe and fatal cases; it has become a cause of concern. The mechanism of HFMD caused by EV71 virus is not completely clear. After it infects host cells, the EV71 virus genome undergoes replication, translation, assembly, and the release of virosomes. Some studies have reported that EV71 could induce host cell autophagy. Autophagy is a cellular process necessary for the lysosomal degradation and recycling of proteins and entire organelles. It can act as not only a defense mechanism to prevent environmental damage to cells, also induce cell death in eukaryotes. To explore the correlation and characteristics of EV71 virus, EV71 viral protein and autophagy, we used EV71 and recombinant plasmid pcDNA3.1 (+)-HA-X to infect human 293T cells, and we found that autophagy could be induced by EV71. With the prolongation of infection, autophagy presents a dynamic trend. And the protein that causes autophagy is structural protein VP1 and non-structural protein 2A.

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The regulation of autophagy in porcine blastocysts: Regulation of PARylation-mediated autophagy via mammalian target of rapamycin complex 1 (mTORC1) signaling

Cited by 10 publications

References 22 publications

Post-Translational Modifications in Oocyte Maturation and Embryo Development

Post-Translational Modifications in Oocyte Maturation and Embryo Development

Curcumin: A naturally occurring autophagy modulator

Characteristics of Autophagy Induced by Enterovirus71 (EV71) Viral Protein

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