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RISS 인기검색어
- 검색키워드
- 저자 : Ma Libing (검색결과 3 건)
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Somatic cell reprogrammed by oocyte: process and barricade
LiBing Ma,XiaoYing He,FengMei Wang,Teng Cheng,XiYu Liu 한국통합생물학회 2014 Animal cells and systems Vol.18 No.3
Somatic cell nuclear transfer (SCNT) is a technology in which a somatic nucleus is transferred into thecytoplasm of a matured oocyte – reconstructed embryos have the capacity to develop to term. Why somaticcells can be reprogrammed by oocytes – the answer for this question must exist in the cytoplasm of maturedoocytes. In this review, totipotent characters of matured oocytes were discussed, which may confer maturedoocytes with the capacity to reprogram somatic nucleus. Moreover, the procedure of SCNT also makes apossibility for somatic nucleus to be reprogrammed by oocytes. Compared with fertilized embryos, embryosderived from SCNT exhibit low developmental ability; the barricades in reprogramming process and theirpossible reasons were also discussed. This review maybe can benefit the mechanism research of SCNTtechnology and can make contribution for improving the efficiency of this technology.
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XiaoYing He,LiBing Ma,Xiao-ning He,Wan-tong Si,Yue-Mao Zheng 대한수의학회 2016 Journal of Veterinary Science Vol.17 No.2
Previous studies have established a bovine mammary gland epithelia cells in vitro model by the adenovirus-mediated telomerase (hTERT-bMGEs). The present study was conducted to confirm whether hTERT-bMGEs were effective target cells to improve the efficiency of transgenic expression and somatic cell nuclear transfer (SCNT). To accomplish this, a mammary-specific vector encoding human lysozyme and green fluorescent protein was used to verify the transgenic efficiency of hTERT-bMGEs, and untreated bovine mammary gland epithelial cells (bMGEs) were used as a control group. The results showed that the hTERT-bMGEs group had much higher transgenic efficiency and protein expression than the bMGEs group. Furthermore, the nontransgenic and transgenic hTERT-bMGEs were used as donor cells to evaluate the efficiency of SCNT. There were no significant differences in rates of cleavage or blastocysts or hatched blastocysts of cloned embryos from nontransgenic hTERT-bMGEs at passage 18 and 28 groups (82.8% vs. 81.9%, 28.6% vs. 24.8%, 58.6% vs. 55.3%, respectively) and the transgenic group (80.8%, 26.5% and 53.4%); however, they were significantly higher than the bMGEs group (71.2%, 12.8% and 14.8%), (p < 0.05). We confirmed that hTERT-bMGEs could serve as effective target cells for improving development of somatic cell cloned cattle embryos.
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The Role of Macrophage Migration Inhibitory Factor (MIF) in Asthmatic Airway Remodeling
Li Ruyi,Wang Feiyun,Wei Jianghong,Lin Yun,Tang Guofang,Rao Lizong,Ma Libing,Xu Qing,Wu Jingjie,Lv Qian,Zhou Rui,Lei Huiren,Zhao Xueqiang,Yao Dong,Xiao Bo,Huang Haiming,Zhang Jiange,Mo Biwen 대한천식알레르기학회 2021 Allergy, Asthma & Immunology Research Vol.13 No.1
Purpose: Recent studies have demonstrated that macrophage migration inhibitory factor (MIF) is of importance in asthmatic inflammation. The role of MIF in modulating airway remodeling has not yet been thoroughly elucidated to date. In the present study, we hypothesized that MIF promoted airway remodeling by intensifying airway smooth muscle cell (ASMC) autophagy and explored the specific mechanisms. Methods: MIF knockdown in the lung tissues of C57BL/6 mice was conducted by instilling intratracheally adeno-associated virus (AAV) vectors (MIF-mutant AAV9) into mouse lung tissues. Mice genetically deficient in the autophagy marker ATG5 (ATG5+/−) was used to detect the role of autophagy in ovalbumin (OVA)-asthmatic murine models. Moreover, to block the expression of MIF and CD74 in vitro models, inhibitors, antibodies and lentivirus transfection techniques were employed. Results: First, MIF knockdown in the lung tissues of mice showed markedly reduced airway remodeling in OVA murine mice models. Secondly, ASMC autophagy was increased in the OVA-challenged models. Mice genetically deficient in the autophagy marker ATG5 (ATG5+/−) that were primed and challenged with OVA showed lower airway remodeling than genetically wild-type asthmatic mice. Thirdly, MIF can induce ASMC autophagy in vitro. Moreover, the cellular source of MIF which promoted ASMC autophagy was macrophages. Finally, MIF promoted ASMC autophagy in a CD74-dependent manner. Conclusions: MIF can increase asthmatic airway remodeling by enhancing ASMC autophagy. Macrophage-derived MIF can promote ASMC autophagy by targeting CD74.
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