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SIRT7 antagonizes human stem cell aging as a heterochromatin stabilizer

Protein & Cell 2020年第7期11卷 483-504页

作者： Shijia Bi Zunpeng Liu Zeming Wu Zehua Wang Xiaoqian liu Si Wang Jie Ren Yan Yao Weiqi Zhang Moshi Song Guang-Hui liu Jing Qu State Key Laboratory of Stem Cell and Reproductive Biology Instiute of ZoologyChinese Academy of SciencesBejing 100101China State Key Laboratory of Membrane Biology Institute of ZoologyChinese Academy of SciencesBejing 100101China Beiing Institute for Brain Disorders Advanced Innovation Center for Human Brain ProtectionNational Clinical Research Center for Geriatric DisordersXuanwu Hospital Capital Medical UniversityBeijing 100053China CAS Key Laboratory of Genomic and Precision Medicine Beiing Institute of GenomicsChinese Academy of SciencesBeijing 100101China China National Center for Bioinformation Bejing 100101China Institute for Stem cell and Regeneration Chinese Academy of SciencesBeiing 100101China University of Chinese Academy of Sciences Beijing 100049China Department of Cardiology Bejing Anzhen HospitalCapital Medical UniversityBeijing 100029China

SIRT7,a sirtuin family member implicated in aging and disease,is a regulator of metabolism and stress responses.It remains elusive how human somatic stem cell populations might be impacted by SIRT7.Here,we found that SIRT7 expression declines during human mesenchymal stem cell(hMSC)aging and that SIRT7 deficiency accelerates senescence.Mechanistically,SIRT7 forms a complex with nuclear lamina proteins and heterochromatin proteins,thus maintaining the repressive state of heterochromatin at nuclear periphery.Accordingly,deficiency of SIRT7 results in loss of heterochromatin,derepression of the LINE1 retrotransposon(LINE1),and activation of innate immune signaling via the cGAS-STING pathway.These agingassociated cellular defects were reversed by overexpression of heterochromatin proteins or treatment with a LINE1 targeted reverse-transcriptase inhibitor.Together,these findings highlight how SIRT7 safeguards chromatin architecture to control innate immune regulation and ensure geroprotection during stem cell aging.

关键词： SIRT7 stem cell aging LINE1 cGAS STING

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Low-dose chloroquine treatment extends the lifespan of aged rats

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Protein & Cell 2022年第6期13卷 454-461页

作者： Wei Li Zhiran Zou Yusheng Cai Kuan Yang Si Wang Zunpeng Liu Lingling Geng Qun Chu Zhejun Ji Piu Chan Guang-Hui liu Moshi Song Jing Qu Weiqi Zhang Advanced Innovation Center for Human Brain Protection National Clinical Research Center for Geriatric DisordersXuanwu Hospital Capital Medical UniversityBeijing 100053China State Key Laboratory of Membrane Biology Institute of ZoologyChinese Academy of SciencesBeijing 100101China State Key Laboratory of Stem Cell and Reproductive Biology Institute of ZoologyChinese Academy of SciencesBeijing 100101China CAS Key Laboratory of Genomic and Precision Medicine Beijing Institute of GenomicsChinese Academy of SciencesBeijing 100101China China National Center for Bioinformation Beijing 100101China Institute for Stem Cell and Regeneration Chinese Academy of SciencesBeijing 100101China University of Chinese Academy of Sciences Beijing 100049China Aging Translational Medicine Center Xuanwu HospitalCapital Medical UniversityBeijing 100053China Beijing Institute for Stem Cell and Regenerative Medicine Beijing 100101China Sino-Danish College University of Chinese Academy of SciencesBeijing 101408China Sino-Danish Center for Education and Research Beijing 101408China Chongqing Renji Hospital University of Chinese Academy of SciencesChongqing 400062China

Dear Editor,Chloroquine(CQ)has long been used as an anti-malarial agent(Wellems and Plowe,2001).Recently,CQ has also been applied to treat viral infection and related diseases(Wellems and Plowe,2001;Huang et al.,2020).However,the safety and efficacy of its applications are still under extensive debate(Solomon and Lee,2009).Here,we discovered that low-dose CQ has a geroprotective effect on physiologically aged rats.Low-dose CQ prolonged lifespan,repressed systemic inflammation,and inhibited fibrosis across multiple tissue types in aged rats.Furthermore,we constructed transcriptomic maps for 6 tissues(kidney,small intestine,liver,heart,lung,and aorta)upon CQ treatment,thus revealing the effects of CQ at a systemic level.CQ treatment mitigated age-related molecular changes and repressed genes linked to fibrosis and the inflammatory response.Altogether,our data provide a valuable resource for investigating the impact of CQ on multiple aged tissues,which may facilitate the development of clinical applications that mitigate age-related changes in the elderly.

关键词： protective inhibited intestine

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Large-scale chemical screen identifies Gallic acid as a geroprotector for human stem cells

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Protein & Cell 2022年第7期13卷 532-539页

作者： Hezhen Shan Lingling Geng Xiaoyu Jiang Moshi Song Jianxun Wang Zunpeng Liu Xiao Zhuo Zeming Wu Jianli Hu Zhejun Ji Si Wang Piu Chan Jing Qu Weiqi Zhang Guang-Hui liu State Key Laboratory of Membrane Biology Institute of ZoologyChinese Academy of SciencesBeijing 100101China State Key Laboratory of Stem Cell and Reproductive Biology Institute of ZoologyChinese Academy of SciencesBeijing 100101China Advanced Innovation Center for Human Brain Protection National Clinical Research Center for Geriatric DisordersXuanwu Hospital Capital Medical UniversityBeijing 100053China CAS Key Laboratory of Genomic and Precision Medicine Beijing Institute of GenomicsChinese Academy of SciencesBeijing 100101China China National Center for Bioinformation Beijing 100101China Institute for Stem Cell and Regeneration Chinese Academy of SciencesBeijing 100101China University of Chinese Academy of Sciences Beijing 100049China Aging Translational Medicine Center Xuanwu HospitalCapital Medical UniversityBeijing 100053China Beijing Institute for Stem Cell and Regenerative Medicine Beijing 100101China Sino-Danish College University of Chinese Academy of SciencesBeijing 101408China School of Life Sciences Beijing University of Chinese MedicineBeijing 100029China

Dear Editor,The interventions that slow aging or promote healthy aging may provide preventative measures for age-related diseases(Zhang et al.,2015).Therefore,it is crucial to identify drugs that target aging-related pathologies and improve health-span in geroscience research.Using model organisms such as C.elegans and rodents,several small molecules capable of alleviating the onset or progression of aging,including rapamycin,nicotinamide mononucleotide,and metformin,have been discovered(Partridge et al.,2020).However,the safety and efficacy of these chemicals still need in-depth evaluation before clinical applications(Partridge et al.,2020).As a result,it is necessary to identify additional compounds with geroprotective effects for human cells to counteract the general trend of populational aging.However,transforming a promising compound into an approved drug requires enormous resources.Alternatively,repurposing previously approved drugs for new clinical applications offers a more efficient and less costly path toward drug develop-ment.Therefore,testing U.S.Food and Drug Administration(FDA)-approved drugs for geroprotective effects may dis-covernew therapeutics that have already been stringently tested in humans for safety.

关键词： drugs protective al.

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FTO stabilizes MIS12 and counteracts senescence

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Protein & Cell 2022年第12期13卷 954-960页

作者： Sheng Zhang Zeming Wu Yue Shi Si Wang Jie Ren Zihui Yu Daoyuan Huang Kaowen Yan Yifang He Xiaoqian liu Qianzhao Ji Beibei liu Zunpeng Liu Jing Qu Guang-Hui liu Weimin Ci Xiaoqun Wang Weiqi Zhang State Key Laboratory of Brain and Cognitive Science CAS Center for Excellence in Brain Science and Intelligence TechnologyInstitute of Brain-Intelligence Technology(Shanghai)Institute of BiophysicsChinese Academy of SciencesBeijing 100101China State Key Laboratory of Membrane Biology Institute of ZoologyChinese Academy of SciencesBeijing 100101China University of Chinese Academy of Sciences Beijing 100049China Institute for Stem Cell and Regeneration Chinese Academy of SciencesBeijing 100101China Beijing Institute for Stem Cell and Regenerative Medicine Beijing 100101China CAS Key Laboratory of Genomic and Precision Medicine Beijing Institute of GenomicsChinese Academy of SciencesBeijing 100101China China National Center for Bioinformation Beijing 100101China Advanced Innovation Center for Human Brain Protection and National Clinical Research Center for Geriatric DisordersXuanwu HospitalCapital Medical UniversityBeijing 100053China Aging Translational Medicine Center International Center for Aging and CancerXuanwu HospitalCapital Medical UniversityBeijing 100053China Chongqing Renji Hospital University of Chinese Academy of SciencesChongqing 400062China Sino-Danish College University of Chinese Academy of SciencesBeijing 101408China State Key Laboratory of Stem Cell and Reproductive Biology Institute of ZoologyChinese Academy of SciencesBeijing 100101China Beijing Institute for Brain Disorders Beijing 100069China

Dear Editor, N6-methyladenosine(m6A)is an abundant epitranscriptomic modification that regulates messenger RNA(mRNA)biology.The m6A modification regulates mRNA splicing,transport,stability,and translation through coordinated activities by methyltransferases(writers),binding proteins(readers),and demethylases(erasers)(Huang et al.,2020;Wu et al.,2020).Among m6A regulators,fat mass of obesity-associ-ated protein(FTO),is the first discovered eraser with RNA m6A demethylation activity(Jia et al.,2011).Since then,FTO has been reported to play m6A-dependent roles in a variety of physiological processes including adipogenesis,neuro-genesis and tumorigenesis(Fischer et al.,2009;Li et al.,2017;Huang et al.,2020).Consequently,FTO deficiency in mice leads to dramatic phenotypes,such as decreased fat mass and impaired brain development(Fischer et al.,2009;Li et al.,2017).Similarly,inhibition of FTO reduces tumori-genesis in multiple types of cancer models,while FTO is highly expressed in many cancers(Huang et al.,2020).

关键词： Fischer impaired

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ALKBH1 deficiency leads to loss of homeostasis in human diploid somatic cells

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Protein & Cell 2020年第9期11卷 688-695页

作者： Hongyu Li Zeming Wu Xiaoqian liu Sheng Zhang Qianzhao Ji Xiaoyu Jiang Zunpeng Liu Si Wang Jing Qu Weiqi Zhang Moshi Song Eli Song Guang-Hui liu National Laboratory of Biomacromolecules CAS Center for Excellence in BiomacromoleculesInstitute of BiophysicsChinese Academy of SciencesBeijing 100101China State Key Laboratory of Stem Cell and Reproductive Biology Institute of ZoologyChinese Academy of SciencesBeijing 100101China State Key Laboratory of Membrane Biology Institute of ZoologyChinese Academy of SciencesBeijing 100101China Institute for Stem Cell and Regeneration Chinese Academy of SciencesBeijing 100101China University of Chinese Academy of Sciences Beijing 100049China Advanced Innovation Center for Human Brain Protection National Clinical Research Center for Geriatric DisordersXuanwu Hospital Capital Medical UniversityBeijing 100053China

Dear Editor,As the most prevalent DNA methylation modification in prokaryotes,DNA N6 methyladenosine(6mA)in eukaryotic genomes has recently been observed in diverse species including Caenorhabditis elegans(Greer et al.,2015),Dro-sophila melanogaster(Zhang et al,2015),mouse(Wu et al,2016)and human(Xiao et al,2018).6mA has been reported to associate with multiple physiological processes including embryonic development and tumorigenesis(Greer et al.,2015;Zhang et al.,2015;Xie et al.,2018),yet some con-troversies exist.In contrast to the findings showing that ALKBH1(alkB homolog 1)is a primary 6mA demethylase in mouse and human cells(Wu et al.,2016;Xiao et al.,2018;Xie et al..2018),other studies indicate that ALKBH1 is prone to demethylate 6mA on bubbled or bulged DNAs that are often featured by a locally unpairing region with flanking duplex,such as D-loop,R-loop as well as DNA or RNA stem-loop,and single-stranded DNAs at a lower efficiency.

关键词： homeostasis bubble pairing

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Low-dose quercetin positively regulates mouse healthspan

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Protein & Cell 2019年第10期10卷 770-775页

作者： Lingling Geng Zunpeng Liu Si Wang Shuhui Sun Shuai Ma Xiaoqian liu Piu Chan Liang Sun Moshi Song Weiqi Zhang Guang-Hui liu Jing Qu Advaneed Innovation Center for Human Brain Protection National Clinical Research Center for Geriatric DisordersXuanwu Hospital Capital Medical UniversityBeijing 100053China State Key Laboratory of Membrane Biology Institute of ZoologyChinese Academy of SciencesBeijing 100101China State Key Laboratory of Stem Cell and Reproductive Biology Institute of ZoologyChinese Academy of SciencesBeijing 100101China Key Laboratory of Genomics and Precision Medicine Beijing Institute of GenomicsChinese Academy of SciencesBeijing 100101China University of Chinese Academy of Sciences Beijing 100049China National Laboratory of Biomacromolecules CAS Center for Excellenee in BiomacromoleculesInstitute of BiophysicsChinese Academy of SciencesBeijing 100101China The MOH Key Laboratory of Geriatrics Beijing HospitalNational Center of GerontologyBeijing 100730China Institute for Stem Cell and Regeneration Chinese Academy of SciencesBeijing 100101China Beijing Institute for Brain Disorders Beijing 100069China

Dear Editor,Aging is the leading risk factor for many chronic diseases,accounting for almost 60%of all deaths worldwide.How to achieve healthy aging,alleviate aging-related diseases,and extend healthspan has become a main topic of biomedical research(He et al.,2019).Geroprotective compounds,such as metformin and rapamycin,have been shown to improve both healthspan and lifespan in mice(Martin-Montalvo et al.,2013;Bitto et al.,2016),whereas nicotinamide partially improves healthspan in mice(Mitchell et al.,2018).

关键词： al. protective diseases

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Single-nucleus transcriptomics reveals a gatekeeper role for FoxP1 in primate cardiac aging

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Protein & Cell 2023年第4期14卷 279-293页

作者： Yiyuan Zhang Yandong Zheng Si Wang Yanling Fan Yanxia Ye Yaobin Jing Zunpeng Liu Shanshan Yang Muzhao Xiong Kuan Yang Jinghao Hu Shanshan Che Qun Chu Moshi Song Guang-Hui liu Weiqi Zhang Shuai Ma Jing Qu National Laboratory of Biomacromolecules CAS Center for Excellence in BiomacromoleculesInstitute of BiophysicsChinese Academy of SciencesBeijing 10o101China State Key Laboratory of Stem Cell and Reproductive Biology Institute of ZoologyChinese Academy of SciencesBeijing 100101China State Key Laboratory of Membrane Biology Institute of ZoologyChinese Academy of SciencesBeijing 100101China University of Chinese Academy of Sciences Beijing100049China Institute for Stem Cell and Regeneration Chinese Academy of SciencesBeijing 100101China Beijing Institute for Stem Cell and Regenerative Medicine Beijing 100101China CAS Key Laboratory of Genomic and Precision Medicine Beijing Institute of GenomicsChinese Academy of SciencesBeijing 100101China China National Center for Bioinformation Beijing 100101China Aging Translational Medicine Center Xuanwu HospitalCapital Medical UniversityBeijing 100053China Advanced Innovation Center for Human Brain Protection National Clinical Research Center for Geriatric DisordersXuanwu Hospital Capital Medical UniversityBeijing 100053China The Fifth People's Hospital of Chongqing Chongqing 400062China Sino-Danish College University of Chinese Academy of SciencesBeijing 101408China

Aging poses a major risk factor for cardiovascular diseases,the leading cause of death in the aged population.However,the cell type-specific changes underlying cardiac aging are far from being clear.Here,we performed single-nucleus RNA-sequencing analysis of left ventricles from young and aged cynomolgus monkeys to define cell composition changes and transcriptomic alterations across different cell types associated with age.We found that aged cardiomyocytes underwent a dramatic loss in cell numbers and profound fluctuations in transcriptional profles.Via transcription regulatory network analysis,we identified FOxP1,a core transcription factor in organ development,as a key downregulated factor in aged cardiomyocytes,concomitant with the dysregulation of FoxP1 target genes associated with heart function and cardiac diseases.Consistently,the deficiency of FOxP1 led to hypertrophic and senescent phenotypes in human embryonic stem cell-derived cardiomyocytes.Altogether,our findings depict the celiular and molecular landscape of ventricular aging at the single-cell resolution,and identify drivers for primate cardiac aging and potential targets for intervention against cardiac aging and associated diseases.

关键词： single-nucleus RNA-sequencing primate aging FOxP1 cardiomyocyte

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DJ-1 is dispensable for human stem cell homeostasis

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Protein & Cell 2019年第11期10卷 846-853页

作者： Fang Cheng Si Wang Moshi Song Zunpeng Liu Ping liu Lei Wang Yanjiang Wang Qian Zhao Kaowen Yan Piu Chan Weiqi Zhang Jing Qu Guang-Hui liu National Laboratory of Biomacromolecules CAS Center for Excellenee in BiomacromoleculesInstitute of BiophysicsChinese Academy of SciencesBeijing 100101China State Key Laboratory of Membrane Biology Institute of ZoologyChinese Academy of SciencesBeijing 100101China State Key Laboratory of Stem Cell and Reproductive Biology Institute of ZoologyChinese Academy of SciencesBeijing 100101China Advaneed Innovation Center for Human Brain Protection National Clinical Research Center for Geriatric DisordersXuanwu Hospital Capital Medical UniversityBeijing 100053China Department of Neurology Daping HospitalThird Military Medical UniversityChongqing 400042China CAS Key Laboratory of Genomic and Precision Medicine Beijing Institute of GenomicsChinese Academy of SciencesBeijing 100101China University of Chinese Academy of Sciences Beijing 100049China Institute for Stem cell and Regeneration Chinese Academy of SciencesBeijing 100101China Translational Medical Center for Stem Cell Therapy Shanghai East HospitalTongji University School of MedicineShanghai 200120China

Dear Editor,Safeguard!ng cellular redox homeostasis is crucial for maintaining organism health and preventing diseases.Oxidative stress,often characterized by decreased mitochondrial integrity and increased reactive oxygen species(ROS)product!on,disrupts proteostasis and genomic stability,which may eventually lead to cellular decomposition(Oh et al.,2014).Stem cells(such as mesenchymal stem cells,MSCs,and neural stem cells,NSCs)are susceptible to various external and internal stresses,and their dysfunction con tributes to aging and agin g-related diseases.Thus,it is of importance to elucidate the complex signaling networks regulated by oxidative stress in stem cells.Although redox signaling has been implicated in multiple cellular processes,how the redox system functions in various human stem cells is unclear.

关键词： PARKINSONS-DISEASE CHCHD2 MUTATIONS REGULATOR

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CRISPR/Cas9-mediated gene knockout reveals a guardian role of NF-κB/RelA in maintaining the homeostasis of human vascular cells

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Protein & Cell 2018年第11期9卷 945-965页

作者： Ping Wang Zunpeng Liu Xiaoqian Zhang Jingyi Li Liang Sun Zhenyu Ju Jian Li Piu Chan Guang-Hui liu Weiqi Zhang Moshi Song Jing Qu National Laboratory of Biomacromolecules CAS Center for Excellence in Biomacromolecules Institute of BiophysicsChinese Academy of Sciences Beijing 100101 China State Key Laboratory of Stem Cell and Reproductive Biology Institute of Zoology Chinese Academy of Sciences Beijing100101 China State Key Laboratory of Membrane Biology Institute of Zoology Chinese Academy of Sciences Beijing 100101 China University of Chinese Academy of Sciences Beijing 100049 China National Clinical Research Center for Geriatric Disorders Xuanwu Hospital of Capital Medical University Beijing 100053China Institute of Stem cell and Regeneration Chinese Academy of Sciences Beijing 100101 China The MOH Key Laboratory of Geriatrics Beijing Hospital National Center of Gerontology Beijing 100730 China Key Laboratory of Regenerative Medicine of Ministry of Education Institute of Aging and Regenerative Medicine JinanUniversity Guangzhou 510632 China

Vascular cell functionality is critical to blood vessel homeostasis. Constitutive NF-κB activation in vascular cells results in chronic vascular inflammation, leading to various cardiovascular diseases. However, how NF-κB regulates human blood vessel homeostasis remains largely elusive. Here, using CRISPR/Cas9-mediated gene editing, we generated RelA knockout human embryonic stem cells （hESCs） and differentiated them into various vascular cell derivatives to study how NF- KS modulates human vascular cells under basal and inflammatory conditions. Multi-dimensional phenotypic assessments and transcriptomic analyses revealed that RelA deficiency affected vascular cells via modulatinginflammation, survival, vasculogenesis, cell differentia- tion and extracellular matrix organization in a cell type- specific manner under basal condition, and that RelA protected vascular cells against apoptosis and modu- lated vascular inflammatory response upon tumor necrosis factor a （TNFa） stimulation. Lastly, further evaluation of gene expression patterns in IKBo knockout vascular cells demonstrated that IKBa acted largely independent of RelA signaling. Taken together, our data reveal a protective role of NF-κB/ReiA in modulating human blood vessel homeostasis and map the human vascular transcriptomic landscapes for the discovery of novel therapeutic targets.

关键词： NF-κB RelA Stem cell Inflammation Apoptosis

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A single-cell transcriptomic atlas of primate pancreatic islet aging

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National Science Review 2021年第2期8卷 17-31页

作者： Jingyi Li Yuxuan Zheng Pengze Yan Moshi Song Si Wang Liang Sun Zunpeng Liu Shuai Ma Juan Carlos Izpisua Belmonte Piu Chan Qi Zhou Weiqi Zhang Guang-Hui liu Fuchou Tang Jing Qu Gene Expression Laboratory Salk Institute for Biological Studies Ministry of Education Key Laboratory of Cell Proliferation and Differentiation National Laboratory of Biomacromolecules CAS Center for Excellence in BiomacromoleculesInstitute of BiophysicsChinese Academy of Sciences Beijing Institute for Brain Disorders Advanced Innovation Center for Human Brain ProtectionNational Clinical Research Center for Geriatric DisordersXuanwu Hospital Capital Medical University The MOH Key Laboratory of Geriatrics Beijing HospitalNational Center of Gerontology Peking-Tsinghua Center for Life Sciences Academy for Advanced Interdisciplinary StudiesPeking University State Key Laboratory of Membrane Biology Institute of ZoologyChinese Academy of Sciences Institute for Stem Cell and Regeneration Chinese Academy of Sciences State Key Laboratory of Stem Cell and Reproductive Biology Institute of ZoologyChinese Academy of Sciences Beijing Advanced Innovation Center for Genomics Biomedical Pioneering Innovation CenterCollege of Life SciencesPeking University CAS Key Laboratory of Genomic and Precision Medicine Beijing Institute of GenomicsChinese Academy of Sciences University of Chinese Academy of Sciences China National Center for Bioinformation

Aging-related degeneration of pancreatic islet cells contributes to impaired glucose tolerance and diabetes.Endocrine cells age heterogeneously, complicating the efforts to unravel the molecular drivers underlying endocrine aging. To overcome these obstacles, we undertook single-cell RNA sequencing of pancreatic islet cells obtained from young and aged non-diabetic cynomolgus monkeys. Despite sex differences and increased transcriptional variations, aged β-cells showed increased unfolded protein response(UPR) along with the accumulation of protein aggregates. We observed transcriptomic dysregulation of UPR components linked to canonical ATF6 and IRE1 signaling pathways, comprising adaptive UPR during pancreatic aging. Notably, we found aging-related β-cell-specific upregulation of HSP90 B1, an endoplasmic reticulum-located chaperone, impeded high glucose-induced insulin secretion. Our work decodes aging-associated transcriptomic changes that underlie pancreatic islet functional decay at single-cell resolution and indicates that targeting UPR components may prevent loss of proteostasis,suggesting an avenue to delaying β-cell aging and preventing aging-related diabetes.

关键词： islet β-cell aging single-cell RNA sequencing primate

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