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Linc-RAM promotes muscle cell differentiation via regulating glycogen phosphorylase activity

Cell Regeneration 2022年第1期11卷 70-83页

作者： Lili Zhai Xin Wan Rimao Wu Xiaohua Yu Hu Li Ran Zhong dahai zhu Yong Zhang The State Key Laboratory of Medical Molecular Biology Institute of Basic Medical SciencesChinese Academy of Medical Sciences and School of Basic MedicinePeking Union Medical CollegeBeijing 100005China Present address:NCPC New Drug Research and Development Co. Ltd.State Key Laboratory of Antibody Research&DevelopmentShijiazhuang 052165China The Max-Planck Center for Tissue Stem Cell Research and Regenerative Medicine Bioland Laboratory(Guangzhou Regenerative Medicine and Health Guangdong Laboratory)Guangzhou 510005China

Long non-coding RNAs(lncRNAs)are important regulators of diverse biological processes,especially skeletal muscle cell *** of the lncRNAs identified to date are localized in the nucleus and play regulatory roles in gene *** cytoplasmic lncRNAs are less well *** previously identified a long intergenic non-coding RNA(linc-RNA)activator of myogenesis(Linc-RAM)that directly binds MyoD in the nucleus to enhance muscle cell ***,we report that a substantial fraction of Linc-RAM is localized in the cytoplasm of muscle *** explore the molecular functions of cytoplasmic Linc-RAM,we sought to identify Linc-RAM-binding *** report here that Linc-RAM physically interacts with glycogen phosphorylase(PYGM)in the *** of PYGM significantly attenuates the function of Linc-RAM in promoting muscle cell ***-of-function and gain-of function assays demonstrated that PYGM enhances muscle cell differentiation in an enzymatic activity-dependent ***,we show that the interaction between Linc-RAM and PYGM positively regulates the enzymatic activity of PYGM in muscle ***,our findings unveil a molecular mechanism through which cytoplasmic Linc-RAM contributes to muscle cell differentiation by regulating PYGM *** findings establish that there is crosstalk between lncRNAs and cellular metabolism during myogenic cell differentiation.

关键词： Muscle cell differentiation Long non-coding RNAs Cytoplasm Linc-RAM Glycogen phosphorylase

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miR-378-mediated glycolytic metabolism enriches the Pax7^(Hi) subpopulation of satellite cells

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Cell Regeneration 2022年第1期11卷 109-118页

作者： Hu Li Lin Kang Rimao Wu Changyin Li Qianying Zhang Ran Zhong Lijing Jia dahai zhu Yong Zhang The Max-Planck Center for Tissue Stem Cell Research and Regenerative Medicine Bioland Laboratory(Guangzhou Regenerative Medicine and Health Guangdong Laboratory)Guangzhou 510005China The State Key Laboratory of Medical Molecular Biology Institute of Basic Medical SciencesChinese Academy of Medical Sciences and School of Basic MedicinePeking Union Medical CollegeBeijing 100005China Department of Endocrinology the Second Clinical Medical College of Jinan UniversityShenzhen People’s HospitalShenzhen 518020China

Adult skeletal muscle stem cells,also known satellite cells(SCs),are a highly heterogeneous population and reside between the basal lamina and the muscle fiber *** function as an immediate niche to support SC self-renewal and activation during muscle growth and ***,we demonstrate that microRNA 378(miR-378)regulates glycolytic metabolism in skeletal muscle fibers,as evidenced by analysis of myofiber-specific miR-378 transgenic mice(TG).Subsequently,we evaluate SC function and muscle regeneration using miR-378 TG *** demonstrate that miR-378 TG mice significantly attenuate muscle regeneration because of the delayed activation and differentiation of ***,we show that the miR-378-mediated metabolic switch enriches Pax7^(Hi) SCs,accounting for impaired muscle regeneration in miR-378 TG ***,our data suggest that miR-378 targets the Akt1/FoxO1 pathway,which contributes the enrichment of Pax7^(Hi) SCs in miR-378 TG ***,our findings indicate that miR-378 is a target that links fiber metabolism to muscle stem cell heterogeneity and provide a genetic model to approve the metabolic niche role of myofibers in regulating muscle stem cell behavior and function.

关键词： satellite cells muscle regeneration miRNAs glycolytic metabolism

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Enhanced metastasis in RNF13 knockout mice is mediated by a reduction in GM-CSF levels

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Protein & Cell 2015年第10期6卷 746-756页

作者： He Cheng Aodi Wang Jiao Meng Yong Zhang dahai zhu The National Laboratory of Medical Molecular Biology Institute of Basic Medical SciencesChinese Academy of Medical Sciences and School of Basic MedicinePeking Union Medical College

RING finger protein 13(RNF13) is a novel E3 ubiquitin ligase whose expression is associated with cancer development. However, its specific role in cancer progression and metastasis remains unclear. Here, a B16F10/LLC experimental pulmonary metastatic model was developed to examine the formation of metastatic foci in the lung. A greater number of tumor colonies were observed in the lungs of RNF13-knockout(KO)mice than in their wild-type(WT) littermates, whereas no significant differences in tumor size were observed between the two groups. In short-term experiments, the number of fluorescently-labeled B16F10 cells increased remarkably in RNF13-KO lungs at early time points,whereas clearance of tumor cells from the blood was not affected. These results indicated that RNF13 may inhibit the colonization of B16F10 cells in the lung. Assessment of the concentration of various cytokines in tumor bearing lungs and blood did not detect significant differences between the blood of RNF13-KO and WT mice;however the levels of GM-CSF were significantly reduced in RNF13-KO tumor bearing lungs, which may have guided more B16F10 cells to migrate to the *** was confirmed by lower GM-CSF concentrations in conditioned media from the culture of RNF13-KO lung slices. Collectively, our results suggest that host RNF13 affects the concentration of GM-CSF in tumor-bearing lungs, leading to a reduction in the colonization of metastatic tumor cells in the lung.

关键词： GM-CSF RNF13 lung cancer metastasis

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Silver Nanowires Contained Nanofluids with Enhanced Optical Absorption and Thermal Transportation Properties

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Energy & Environmental Materials 2019年第1期2卷 22-29页

作者： dahai zhu Guiwen Huang Liye Zhang Yan He Huaqing Xie Wei Yu School of Environmental and Materials Engineering College of EngineeringShanghai Polytechnic UniversityShanghai 201209China Technical Institute of Physics and Chemistry Chinese Academy of SciencesBeijing 100190China School of Mechanical and Electrical Engineering Qingdao University of Science and TechnologyQingdao 266061China Shanghai Innovation Institute for Materials Shanghai 200444China

Two kinds of silver nanowires(100 nm in diameter, 20 μm and 100 μm in length) are prepared. The thermo-physical characteristics, viscosity, and photothermal conversion performance of the silver nanowires(AgNWs)contained ethylene glycol nanofluids are investigated in detail. It is found that thermal conductivity of 100 μm AgNWs contained nanofluids is higher than that of 20 μm AgNWs with the same diameters of 100 nm. Viscosity test shows that the nanofluid is a Newtonian fluid, and the longer silver nanowires, the greater viscosity. In addition, photothermal conversion efficiency of silver nanowires contained nanofluid is studied. We can observe that the 100 μm AgNWs contained nanofluid has a higher photothermal conversion efficiency than that containing 20 μm AgNWs. Moreover, we find that there is a certain correlation between heat transfer and photothermal conversion of nanofluid. It demonstrates that the high heat transfer property of nanofluid will benefit for its photothermal conversion efficiency and the mechanism is proposed. This work provides a new idea to improve photothermal conversion efficiency. We can choose materials with high thermal conductivity and strong light absorption ability to enhance the photothermal conversion performance of nanofluids.

关键词： nanofluid photothermal property silver nanowires thermal conductivity

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Accelerated regeneration of the skeletal muscle in RNF13-knockout mice is mediated by macrophage-secreted IL-4/IL-6

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Protein & Cell 2014年第3期5卷 235-247页

作者： Jiao Meng Xiaoting Zou Rimao Wu Ran Zhong dahai zhu Yong Zhang The National Laboratory of Medical Molecular Biology Institute of Basic Medical Sciences Chinese Academy of MedicalSciences and School of Basic Medicine Peking Union Medical College Beijing 100005 China

RING finger protein 13 （RNF13） is a newly identified E3 ligase reported to be functionally significant in the reg- ulation of cancer development, muscle cell growth, and neuronal development. In this study, the function of RNF13 in cardiotoxin-induced skeletal muscle regener- ation was investigated using RNF13-knockout mice. RNF13-/- mice exhibited enhanced muscle regeneration --characterized by accelerated satellite cell proliferation --compared with wild-type mice. The expression of RNF13 was remarkably induced in macrophages rather than in the satellite cells of wild-type mice at the very early stage of muscle damage. This result indicated that inflammatory cells are important in RNF13-mediated satellite cell functions. The cytokine levels in skeletal muscles were further analyzed and showed that RNF13＂i＂ mice produced greater amounts of various cytokines than wild-type mice. Among these, IL-4 and IL-6 levels significantly increased in RNF13-/＂ mice. The accelerated muscle regeneration phenotype was abrogated by inhibiting IL-4/IL-6 action in RNF13＂/- mice with blocking antibodies. These results indicate that RNF13 deficiency promotes skeletal muscle regeneration via the effects on satellite cell niche mediated by IL-4 and IL-6.

关键词： RNF13 muscle regeneration satellite celniche. IL-4/IL-6

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Threonine 32 （Thr32） of FoxO3 is critical for TGF-β-induced apoptosis via Bim in hepatocarcinoma cells

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Protein & Cell 2015年第2期6卷 127-138页

作者： Xiangxuan Zhao Yong Liu Lei Du Leya He Biyun Ni Junbo Hu dahai zhu Quan Chen The Joint Laboratory of Apoptosis and Cancer Biology The State Key Laboratory of Biomembrane and Membrane Biotechnology Institute of Zoology Chinese Academy of Sciences Beijing 100101 China University of Chinese Academy of Sciences Beijing 100049 China Department of Radiology Shengjing Hospital of China Medical University Shenyang 110004 China Cancer Research Center Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430032 China Institute of Basic Medical Sciences of Chinese Academy of Medical Sciences and School of Basic Medicine of Peking Union Medical College Beijing 100005 China College of Life Science Nankai University Tianjin 300071 China

Transforming growth factor-β （TGF-β） exerts apoptotic effects on various types of malignant ceils, including liver cancer cells. However, the precise mechanisms by which TGF-β induces apoptosis remain poorly known. In the present study, we have showed that threonine 32 （Thr32） residue of FoxO3 is critical for TGF-β to induce apoptosis via Bim in hepatocarcinoma Hep3B cells. Our data demonstrated that TGF-βinduced FoxO3 activation through specific de-phosphorylation at Thr32. TGF-β-activated FoxO3 cooperated with Smad2/ 3 to mediate Bim up-regulation and apoptosis. FoxO3 （de）phosphorylation at Thr32 was regulated by casein kinase I-ε （CKI-E）. CKI inhibition by small molecule D4476 could abrogate TGF-β-induced FoxO/Smad acti- vation, reverse Bim up-regulation, and block the sequential apoptosis. More importantly, the deregulated levels of CKI-ε and p32FoxO3 were found in human malignant liver tissues. Taken together, our findings suggest that there might be a CKI-FoxO/Smad-Bim engine in which Thr32 of FoxO3 is pivotal for TGF-β- induced apoptosis, making it a potential therapeutic target for liver cancer treatment.

关键词： apoptosis TGF-β FoxO3 casein kinasel-ε hepatocarcinoma

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New insights into the functions and signaling pathways of myostatin in regulating cell proliferation and metabolisms

New insights into the functions and signaling pathways of my...

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中国生物化学与分子生物学会第十届会员代表大会暨全国学术...

作者： dahai zhu National Laboratory of Medical Molecular Biology Department of Biochemistry and Molecular BiologyInstitute of Basic Medical SciencesChinese Academy of Medical Sciences & Peking Union Medical College

Myostatin,also named GDF-8(Growth and Differentiation Factor-8),is a member of the TGF-fi superfamily and has been emerged as a important regulator of skeletal muscle *** gene is highly conserved in mammalian *** in cattle,sheep,dogs,and one child cause an dramatic increase in skeletal muscle mass,suggesting that myostatin normally acts as a negative regulator of muscle *** work from my laboratory has demonstrated that Myostatin could inhibits myoblast cell proliferation through Erkl/2 and PI3K/Akt/GSK3b ***

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Skeletal Muscle-Secreted Lipids Regulates Metabolic Homeostasis by Mediating Muscle-Fat Crosstalk

Skeletal Muscle-Secreted Lipids Regulates Metabolic Homeosta...

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中国生物化学与分子生物学会2019年全国学术会议暨学会...

作者： dahai zhu The State Key Laboratory of Medical Molecular Biology Institute of Basic Medical Sciences Chinese Academy of Medical Sciences and School of Basic Medicine Peking Union Medical College Max-Planck Center for Tissue Stem Cell Research and Regenetive Medicine GDL

Skeletal muscles play central roles in orchestrating organismal energy homeostasis. However, the molecular mechanisms underlying this globally metabolic regulation of skeletal muscle remain a conundrum. Increasing lines of evidence have demonstrated the functional significance of skeletal muscle-secreted factors in regulating whole body energy homeostasis by actively communicating with other metabolic organs such as fat and liver. Only a few numbers of the the muscle-secreted factors with the metabolicaly regulatory role have been reported. Therefore it is critical to identify the muscle-secreted factors in order to understanding the molecular mechaism of skeletal muscle in orchestrating inter-organ crostalk and developing potential drug for treating metabolic diseases such as obesity and type Ⅱ diabetes mellitus. Herein, we for the first time demonstrate skeletal muscle-released lipids functionally involve musclefat crosstalk to attenuate HFD-induced obesity by inducing white fat browning. The findings uncover the unanticipated role that lipid species serve as a promising agent for preventing and treating obesity in humans.

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Enhanced metastasis in RNF13 knockout mice s mediated by a reduction in GM-CSF levels

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Protein & Cell 2015年第10期6卷 746-756页

作者： He Cheng Aodi Wang Jiao Meng Yong Zhang dahai zhu The National Laboratory of Medical Molecular Biology Institute of Basic Medical Sciences Chinese Academy of MedicalSciences and School of Basic Medicine Peking Union Medical College Beijing 100005 China

RING finger protein 13 （RNF13） is a novel E3 ubiquitin ligase whose expression is associated with cancer development. However, its specific role in cancer progression and metastasis remains unclear. Here, a B16F10/LLC experimental pulmonary metastatic model was developed to examine the formation of metastatic foci in the lung. A greater number of tumor colonies were observed in the lungs of RNF13-knockout （KO） mice than in their wild-type （WT） littermates, whereas no significant differences in tumor size were observed between the two groups. In short-term experiments, the number of fluorescently-labeled B16F10 cells increased remarkably in RNF13-KO lungs at early time points, whereas clearance of tumor cells from the blood was not affected. These results indicated that RNF13 may inhibit the colonization of B16F10 cells in the lung. Assessment of the concentration of various cytokines in tumor bearing lungs and blood did not detect significant dif- ferences between the blood of RNF13-KO and WT mice; however the levels of GM-CSF were significantly reduced in RNF13-KO tumor bearing lungs, which may have guided more B16F10 cells to migrate to the lungs. This was confirmed by lower GM-CSF concentrations in conditioned media from the culture of RNF13-KO lung slices. Collectively, our results suggest that host RNF13 affects the concentration of GM-CSF in tumor-bearing lungs, leading to a reduction in the colonization of metastatic tumor cells in the lung.

关键词： RNF13 metastasis GM-CSF lung cancer

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花楸属直脉组7种/变种基因组大小及叶表皮微形态特征的分类学意义

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南京林业大学学报（自然科学版） 2023年第3期47卷 77-86页

作者：邱靖李嘉宝朱大海陈昕南京林业大学南方现代林业协同创新中心南京林业大学生物与环境学院江苏南京210037 三江学院江苏南京210012 龙溪-虹口国家级自然保护区四川成都611830

【目的】通过对花楸属直脉组(Sorbus ***)5种及具有分类争议的2变种的基因组大小和叶表皮微形态研究,探讨其分类学意义以及基因组大小和细胞大小之间的相关性。【方法】基于流式细胞术、光学和电子显微镜分别对研究对象的基因组大小、... 详细信息

【目的】通过对花楸属直脉组(Sorbus ***)5种及具有分类争议的2变种的基因组大小和叶表皮微形态研究,探讨其分类学意义以及基因组大小和细胞大小之间的相关性。【方法】基于流式细胞术、光学和电子显微镜分别对研究对象的基因组大小、叶表皮细胞和气孔的质量和数量性状进行测定、分析。【结果】基因组大小测定显示所有分类群均为极小基因组,大小介于神农架花楸(***)的1.348 pg至长果花楸(***)的1.586 pg之间;虽均为二倍体,但分类群间基因组大小差异显著。光学显微镜下叶表皮细胞形状兼有多边形和无规则形,或者仅无规则形,垂周壁式样有平直状、弧状和波状;扫描电镜下表皮纹饰有近光滑、局部加厚、脊状、网纹、褶皱等类型,蜡质纹饰有壳状、颗粒状、线状、片状等;4个分类群的下表皮具带状单毛。气孔器均为无规则型,分布于下表皮脉间区;保卫细胞具明显的环形外缘或无。表皮细胞面积、气孔宽度及面积、气孔密度、气孔指数等指标在分类群间差异显著,基因组大小同表皮细胞面积、气孔长宽及面积呈正相关,同气孔密度和气孔指数呈负相关。【结论】基因组大小、叶表皮微形态质量和数量性状可为7个分类群的鉴定提供依据,不支持将棱果花楸(*** ***)和裂叶水榆花楸(***)作为日本花楸(*** ***)的异名处理,建议恢复棱果花楸和裂叶水榆花楸的名称。

关键词：基因组大小细胞大小微形态特征叶表皮花楸属直脉组

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