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Protective Effects of C-phycocyanin on Developmental Competence of Pig Parthenotes
Ying-Jie Niu,Jing Guo,Kyung-Tae Shin,Nam-Hyung Kim,Xiang-Shun Cui 한국동물생명공학회(구 한국동물번식학회) 2017 Reproductive & Developmental Biology(Supplement) Vol.41 No.2
C-phycocyanin (C-PC) is a biliprotein enriched in blue-green algae that is known to possess antioxidant, antiapoptosis, anti-inflammatory, and radical-scavenging properties in somatic cells. But the protective effect of C-PC on porcine embryo developmental competence in in vitro is little known. In the present study, we investigated the effect of C-PC on the development of porcine early embryos as well as the underlying its mechanisms. Different concentrations of C-CP (1, 2, 5, 8, 10 μg/mL) was added to the porcine zygote medium 5 (PZM-5) during in vitro culture. The results showed that 5 μg /mL C-PC significantly increased blastocyst formation. Blastocyst formation and its quality were significantly increased in 50 μM H2O2 treatment group following 5 μg/mL C-PC addition. C-PC prevented H2O2-induced compromise of mitochondrial membrane potential, release of cytochrome c from the mitochondria and reactive oxygen species generation. Furthermore, apoptosis, DNA damage level and autophagy in the blastocysts were attenuated by supplement of C-PC in H2O2-induced oxidative injury group compared with control. Taken together, these results suggest that C-PC has beneficial effects on the development of porcine parthenotes by attenuating mitochondrial dysfunction and oxidative stress.
Ying-Jie Niu,Kyung-Tae Shin,Wenjun Zhou,Zheng-Wen Nie,Junchul David Yoon,Nam-Hyung Kim,Xiang-Shun Cui 한국동물생명공학회(구 한국동물번식학회) 2017 발생공학 국제심포지엄 및 학술대회 Vol.2017 No.10
C-phycocyanin (C-PC) is a biliprotein enriched in blue-green algae that is known to possess antioxidant, antiapoptosis, anti-inflammatory, and radical-scavenging properties in somatic cells. But the protective effect of C-PC on porcine embryo developmental competence in in vitro is little known. In the present study, we investigated the effect of C-PC on the development of porcine early embryos as well as the underlying its mechanisms. Different concentrations of C-CP (1, 2, 5, 8, 10 μg/mL) was added to the porcine zygote medium 5 (PZM-5) during in vitro culture. The results showed that 5 μg/mL C-PC significantly increased blastocyst formation. Blastocyst formation and its quality were significantly increased in 50 μM H2O2 treatment group following 5μg/mL C-PC addition. C-PC prevented H2O2-induced compromise of mitochondrial membrane potential, release of cytochrome C from the mitochondria and reactive oxygen species generation. Furthermore, apoptosis, DNA damage level and autophagy in the blastocysts were attenuated by supplement of C-PC in H2O2-induce doxidativ injury group compared with control.Taken together, these results suggest that C-PC has beneficial effects on the development of porcine parthenotes by attenuating mitochondrial dysfunction and oxidative stress.
Niu, Ying-Jie,Zhou, Dongjie,Zhou, Wenjun,Nie, Zheng-Wen,Kim, Ju-Yeon,Oh, YoungJin,Lee, So-Rim,Cui, Xiang-Shun The Korean Society of Animal Reproduction and Biot 2020 한국동물생명공학회지 Vol.35 No.1
Nitric oxide (NO)-induced protein S-nitrosylation triggers mitochondrial dysfunction and was related to cell senescence. However, the exact mechanism of these damages is not clear. In the present study, to investigate the relationship between in vitro aging and NO-induced protein S-nitrosylation, oocytes were treated with sodium nitroprusside dihydrate (SNP), and the resultant S-nitrosylated proteins were detected through biotin-switch assay. The results showed that levels of protein S-nitroso thiols (SNO)s and expression of S-nitrosoglutathione reductase (GSNOR) increased, while activity and function of mitochondria were impaired during oocyte aging. Addition of SNP, a NO donor, to the oocyte culture led to accelerated oocyte aging, increased mitochondrial dysfunction and damage, apoptosis, ATP deficiency, and enhanced ROS production. These results suggested that the increased NO signal during oocyte aging in vitro, accelerated oocyte degradation due to increased protein S-nitrosylation, and ROS-related redox signaling.
Melatonin enhances mitochondrial biogenesis and function in porcine preimplantation embryos
Ying-Jie Niu,Wenjun Zhou,Zheng-Wen Nie,Kyung-Tae Shin,Yong-Han Kim,Xiang-Shun Cui 한국수정란이식학회 2018 한국수정란이식학회 학술대회 Vol.2018 No.11
Melatonin (N-aceyl-5-methoxytryptamine) is the major hormone of the pineal gland. Melatonin and its metabolic derivatives possess extensive free-radical scavenging abilities and played critical roles in antioxidative stress, resisting apoptotic cell death. Melatonin also could enhance mitochondrial biogenesis in rats with carbon tetrachloride-induced liver fibrosis. In addition, melatonin attenuates myocardial ischemia/reperfusion injury by reducing oxidative stress damage via activation of SIRT1 signaling in a melatonin receptor 2-dependent manner. Activation or overexpression of SIRT1 could enhance mitochondrial biogenesis and function by inducing PGC-1α expression and deacetylation. The aim of this study was to investigate if melatonin enhances mitochondrial biogenesis and function via activation of melatonin receptor 2/SIRT1/PGC1-α Pathway. The results showed that Melatonin rescued rotenone-induced impairment of porcine embryo development. Treatment with rotenone could increase oxidative stress and apoptosis. Rotenone impaired mitochondrial functions by disrupting mitochondrial membrane potential, reducing mitochondrial DNA copy number and ATP production. Melatonin could improve SIRT1 and PGC-1α expression, inducing mitochondrial biogenesis. Rotenone-induced mitochondrial dysfunction and ATP deficiency was rescued by melatonin treatment, the oxidative stress and apoptosis was significantly decreased. Inhibition of melatonin receptor 2 or Knockdown of SIRT1 abolished the protective effects of melatonin on rotenone-induced impairments. Therefore, melatonin enhanced mitochondrial biogenesis and function, protected against rotenone-induced impairments.
TIP60 Contributes to DNA Damage Repair during Early Embryonic Development in Pig
Ying-Jie Niu,Jing Guo,Kyung-Tae Shin,Nam-Hyung Kim,Xiang-Shun Cui 한국수정란이식학회 2017 한국수정란이식학회 학술대회 Vol.2017 No.05
The acetyltransferase Tip60 (Kat5) is a member of the MYST family of HATs that was initially identified as a cellular protein. TIP60 acetylates histone and non-histone proteins, and is involved in diverse biological processes, including apoptosis, cell cycle, and DNA damage responses. In this study, a specific inhibitor of TIP60, Nu 9056, was used to study the function and its regulatory mechanism of Tip60 in the porcine preimplantation embryonic development. The results showed that inhibition of TIP60 impaired the embryonic development due to induce DNA damage through ATM-p53-p21 pathway, it was evidenced by expression of γH2A in the nuclei of blastocysts. In addition, TIP60 inhibition decreased efficiency of DNA repair by regulating P53 binding protein 1 expression. Furthermore, autophagy was induced following TIP60 inhibition through modulating microtubule-associated protein 1A/1B-light chain 3 expression. In conclusion, the results suggest that TIP60 plays a critical role in early embryonic development via regulation of DNA damage and its repairs.
Ying-Jie Niu,Dongjie Zhou,Wenjun Zhou,Zheng-Wen Nie,Ju-Yeon Kim,YoungJin Oh,So-Rim Lee,Xiang-Shun Cui 한국동물생명공학회(구 한국동물번식학회) 2020 Journal of Animal Reproduction and Biotechnology Vol.35 No.1
Nitric oxide (NO)-induced protein S-nitrosylation triggers mitochondrial dysfunction and was related to cell senescence. However, the exact mechanism of these damages is not clear. In the present study, to investigate the relationship between in vitro aging and NO-induced protein S-nitrosylation, oocytes were treated with sodium nitroprusside dihydrate (SNP), and the resultant S-nitrosylated proteins were detected through biotin-switch assay. The results showed that levels of protein S-nitroso thiols (SNO)s and expression of S-nitrosoglutathione reductase (GSNOR) increased, while activity and function of mitochondria were impaired during oocyte aging. Addition of SNP, a NO donor, to the oocyte culture led to accelerated oocyte aging, increased mitochondrial dysfunction and damage, apoptosis, ATP deficiency, and enhanced ROS production. These results suggested that the increased NO signal during oocyte aging in vitro, accelerated oocyte degradation due to increased protein S-nitrosylation, and ROS-related redox signaling.
Sheng-jie Niu,Qiu-ying Zhang 한국기상학회 2010 Asia-Pacific Journal of Atmospheric Sciences Vol.46 No.1
The authors investigated variations of aerosol scattering and absorptive properties in a semi-arid climate Observatory in the Inner Mongolia of China and factors affecting the variation. They use integrated nephelometer and aethalometer observations collected in 2005 and 2006 at the Silinhot Observatory. The results are as follows. 1) in autumn and winter, the diurnal cycle of scattering coefficient exhibited a clear bi-modal variation, and the scattering coefficient was indicative of the type of sandy weather. 2) The concentration of black carbon (BC) aerosols was much higher in winter than in the other seasons with an evident bimodal diurnal variation. 3) When the wind speed was lower than 3.5 m s-1, the dilution effect of air evidently influenced the scattering coefficient and BC mass concentration; for the wind speed above 3.5 m s-1, there appeared to be little correlation between wind speed and scattering coefficient or BC mass concentration. 4) Atmospheric visibility calculated from the aerosol scattering and absorptive coefficients was in good agreement with the direct observation of visibility. 5) Absorption by aerosols accounted for 25% of the total extinction in December.
Knockout of Fatty Acid Synthase induces Endoplasmic Reticulum Stress in Porcine Early Embryos
Jing Guo,Ying-Jie Niu,Kyung-Tae Shin,Nam-Hyung Kim,Xiang-Shun Cui 한국동물생명공학회(구 한국동물번식학회) 2017 Reproductive & Developmental Biology(Supplement) Vol.41 No.2
Fatty acid synthase (FASN) is an enzyme that catalyzes the synthesis of long chain fatty acid. During development, FASN plays a role in growth rather than the energy storage pathways. In this study, we hypothesis that knockout of FASN may affect the early embryonic development through induction of the endoplasmic reticulum (ER) stress. The function of FASN was studied using the Crispr/Cas9 technology. We found that FASN knockout induced ER stress by generation of reactive oxygen species (ROS), further resulted in the activation of adaptive unfolded protein response (UPR), caused the splicing of XBP1. In addition, FASN knockout increased ATF4 and CHOP expression, influenced phosphorylation of PERK. At last, Ca2+ was released from the ER and then taken up by the mitochondrial and influenced mitochondrial function, initiated apoptosis. These results demonstrated that FASN knockout induced generation of ROS, which mediated the activation of UPR via the ER and subsequent apoptosis in porcine early embryos.