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RISS 인기검색어
- 검색키워드
- 저자 : Ruyi Li (검색결과 3 건)
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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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Guojun Ke,Wengui Li,Ruyi Li,Yuelin Li,George Wang 한국콘크리트학회 2018 International Journal of Concrete Structures and M Vol.12 No.7
The effects of different contents and particle sizes of waste glass powder on alkali–silica reaction (ASR) expansion of cementitious composite bar were investigated in this study. Waste glass powder with particle size less than 300 ㎛ exhibits an excellent mitigation effect on ASR expansion. With larger content and smaller particle size, the mitigation effect of waste glass powder on ASR expansion gradually increases. The mitigation effect of waste glass powder with particle size ranging from 38 to 53 ㎛ and 20% by weight of cement seems relatively better than that of fly ash. When the waste glass powder content reaches 30%, the mitigation effect is still effective and almost the same as that of fly ash. However, the waste glass powder with particle size larger than 300 ㎛ presents negative mitigation effect on ASR expansion when the replacement rate is larger than 30%. On the other hand, the waste glass powder and calcium hydroxide (CH) further react, and produce more calcium–silicate–hydrate gels, which apparently reduce the amount of CH. Moreover, the increasing content of waste glass powder results in a lower pH value in the pore solution of cementitious composite.
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Dandan Zhang,Cuixia Gao,Ruyi Li,Lin Zhang,Jingkui Tian 대한약학회 2017 Archives of Pharmacal Research Vol.40 No.5
2a,3a,24-Thrihydroxyurs-12-en-28-oicacid (TEOA),a pentacyclic triterpenoid, isolated from the roots of Actinidiaeriantha, exhibits significant cytotoxicity against SW620, BGC-823, HepG-2, A549 and PC-3 cancer cells. In this study, weinvestigated the underlying molecular mechanism of the anticanceractivity of TEOA in SW620 cells.We demonstrated thatTEOA induced apoptosis through cleavage of caspase-9 andPARP in SW620 cells. In addition, evidence of TEOA-mediatedautophagy included the induction of autophagolysosomesand activation of autophagic markers LC-3B and p62. Furtheranalysis illustrated that TEOA promoted the phosphorylation ofPERK and elF2a, followed by up-regulation of the downstreamprotein CHOP, suggesting the involvement of PERK/eIF2a/CHOP pathway and ER stress in TEOA-induced autophagy inSW620 cells. Meanwhile, TEOA-mediated PINK1, Parkin,ubiquitin and p62 activation revealed that TEOA inducedspecific autophagy-mitophagy in SW620 cells. Additionally, anantioxidant NAC attenuated the TEOA-induced mitophagy,indicating that TEOA triggers mitophagy via a ROS-dependentpathway. Collectively, our findings revealed a novel cellularmechanism of TEOA in the colon cancer cell line SW620, thusproviding a molecular basis for developing TEOA into an antitumorcandidate.
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