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您的检索式：作者名="Ruoyu Duan"
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| 1 | Superresolution live-cell imaging reveals that the localization of TMEM106B to filopodia in oligodendrocytes is compromised by the hypomyelination-related D252N mutation显示文摘Hypomyelination leukodystrophies constitute a group of heritable white matter disorders exhibiting defective myelin development.Initially identified as a lysosomal protein,the TMEM106B D252N mutant has recently been associated with hypomyelination.However,how lysosomal TMEM106B facilitates myelination and how the D252N mutation disrupts that process are poorly understood.We used superresolution Hessian structured illumination microscopy(Hessian-SIM)and spinning discconfocal structured illumination microscopy(SD-SIM)to find that the wild-type TMEM106B protein is targeted to the plasma membrane,filopodia,and lysosomes in human oligodendrocytes.The D252N mutation reduces the size of lysosomes in oligodendrocytes and compromises lysosome changes upon starvation stress.Most importantly,we detected reductions in the length and number of filopodia in cells expressing the D252N mutant.PLP1 is the most abundant myelin protein that almost entirely colocalizes with TMEM106B,and coexpressing PLP1 with the D252N mutant readily rescues the lysosome and filopodia phenotypes of cells.Therefore,interactions between TMEM106B and PLP1 on the plasma membrane are essential for filopodia formation and myelination in oligodendrocytes,which may be sustained by the delivery of these proteins from lysosomes via exocytosis. | Shijia Xing Xiaolu Zheng Huifang Yan Yanquan Mo Ruoyu Duan Zhixing Chen Kunhao Wang Kai Gao Tongsheng Chen Shiqun Zhao Jingmin Wang Liangyi Chen | 2023 | Science China(Life Sciences)2023，66，8： | 0 |
| 2 | The proatherosclerotic function of indoleamine 2, 3- dioxygenase 1 in the developmental stage of atherosclerosis显示文摘The discrepancy of indoleamine 2,3-dioxygenase 1(IDO1)function in atherosclerosis has been noted.Compared to the protective effect of IDO1 against established atherogenesis,the role of IDO1 in the developmental process of atherosclerosis is still unclear.Here,the expression patterns and activities of IDO1 and its isoenzyme tryptophan 2,3-dioxygenase(TDO)in aortas and blood samples of patients with atherosclerosis were investigated.IDO1 and TDO were colocalized with CD3-positive lymphocytes and CD68-positive macrophages in atherosclerotic lesions.The expression and activity of IDO1 and TDO increased with the grade of the histological classification in early atherosclerosis(grade I,II),but the increase did not continue in advanced atherosclerosis(grade III).Treatment of THP-1 macrophages(THP-M)with oxidized low-density lipoprotein(oxLDL)induced the expression of IDO1 via the PI3K/Akt/NF-κB pathway,indicating the potential function of IDO1 in foam cells.Before and after treatment with oxLDL on THP-M,IFN-γ-induced IDO1 exhibited different degrees of promotion on foaming,inflammatory factor production and cell apoptosis.Finally,we found that the IDO1 inhibitor 1-methyl-tryptophan could elevate the high-density lipoprotein cholesterol level in serum and reduce the area of the aortic atherosclerotic lesions in high-fat diet-fed ApoE−/−mice.Our study indicated that IDO1 played a complicated and unfixed role in the entire process of atherogenesis,despite the atheroprotective role in established atherosclerosis.IDO1 also had proatherosclerotic functions in the developmental stages of atherosclerosis.Modulation of IDO1 could be a good method for alleviating atherosclerosis. | Heng Liang Mantian Chen Fangfei Qi Lei Shi Zhenzhen Duan Ruoyu Yang Jinchao He Bin Lou Yigang Li Qing Yang | 2019 | Signal Transduction and Targeted Therapy2019，4，1： | 0 |
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