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A pancreatic player in dementia:pathological role for islet amyloid polypeptide accumulation in the brain

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Neural Regeneration research 2023年第10期18卷 2141-2146页

作者： Angelina S.Bortoletto Ronald J.Parchem center for cell and Gene Therapy Stem Cell and Regenerative Medicine CenterDepartment of NeuroscienceDepartment of Molecular and Cellular BiologyTranslational Biology and Molecular Medicine ProgramMedical Scientist Training ProgramBaylor College of MedicineHoustonTXUSA

Type 2 diabetes mellitus patients have a markedly higher risk of developing dementia.While multiple factors contribute to this predisposition,one of these involves the increased secretion of amylin,or islet amyloid polypeptide,that accompanies the pathophysiology of type 2 diabetes mellitus.Islet amyloid polypeptide accumulation has undoubtedly been implicated in various forms of dementia,including Alzheimer’s disease and vascular dementia,but the exact mechanisms underlying islet amyloid polypeptide’s causative role in dementia are unclear.In this review,we have summarized the literature supporting the various mechanisms by which islet amyloid polypeptide accumulation may cause neuronal damage,ultimately leading to the clinical symptoms of dementia.We discuss the evidence for islet amyloid polypeptide deposition in the brain,islet amyloid polypeptide interaction with other amyloids implicated in neurodegeneration,neuroinflammation caused by islet amyloid polypeptide deposition,vascular damage induced by islet amyloid polypeptide accumulation,and islet amyloid polypeptide-induced cytotoxicity.There are very few therapies approved for the treatment of dementia,and of these,clinical responses have been controversial at best.Therefore,investigating new,targetable pathways is vital for identifying novel therapeutic strategies for treating dementia.As such,we conclude this review by discussing islet amyloid polypeptide accumulation as a potential therapeutic target not only in treating type 2 diabetes mellitus but as a future target in treating or even preventing dementia associated with type 2 diabetes mellitus.

关键词： Alzheimer’s disease amylin amyloid dementia diabetes human islet amyloid polypeptide islet amyloid polypeptide protofibrils type 2 diabetes mellitus vascular dementia

PIWI proteins and their interactors in piRNA biogenesis,germline development and gene expression

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National Science Review 2014年第2期1卷 205-218页

作者： Hsueh-Yen Ku Haifan Lin Yale stem cell center and department of cell biology Yale University School of Medicine

PIWI-interacting RNAs(piRNAs) are a complex class of small non-coding RNAs that are mostly 24–32nucleotides in length and composed of at least hundreds of thousands of species that speciically interact with the PIWI protein subfamily of the ARGONAUTE family. Recent studies revealed that PIWI proteins interact with a number of proteins, especially the TUDOR-domain-containing proteins, to regulate piRNA biogenesis and regulatory function. Current research also provides evidence that PIWI proteins and pi RNAs are not only crucial for transposon silencing in the germline, but also mediate novel mechanisms of epigenetic programming, DNA rearrangements, m RNA turnover, and translational control both in the germline and in the soma. hese new discoveries begin to reveal an exciting new dimension of gene regulation in the cell.

关键词： PIWI piRNA TDRD epigenetic RNA decay translational regulation

Intermittent compressive force induces cell cycling and reduces apoptosis in embryoid bodies of mouse induced pluripotent stem cells

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International Journal of Oral Science 2022年第1期14卷 40-50页

作者： Jeeranan Manokawinchoke Phoonsuk Limraksasin Hiroko Okawa Prasit Pavasant Hiroshi Egusa Thanaphum Osathanon Division of Molecular and Regenerative Prosthodontics Tohoku University Graduate School of DentistrySendaiMiyagiJapan Dental stem cell biology research Unit and department of Anatomy Faculty of DentistryChulalongkorn UniversityBangkokThailand center for Advanced stem cell and Regenerative research Tohoku University Graduate School of DentistrySendaiMiyagiJapan

In vitro manipulation of induced pluripotent stem cells(iPSCs) by environmental factors is of great interest for three-dimensional(3D) tissue/organ induction. The effects of mechanical force depend on many factors, including force and cell type. However,information on such effects in i PSCs is lacking. The aim of this study was to identify a molecular mechanism in i PSCs responding to intermittent compressive force(ICF) by analyzing the global gene expression profile. Embryoid bodies of mouse i PSCs, attached on a tissue culture plate in 3D form, were subjected to ICF in serum-free culture medium for 24 h. Gene ontology analyses for RNA sequencing data demonstrated that genes differentially regulated by ICF were mainly associated with metabolic processes,membrane and protein binding. Topology-based analysis demonstrated that ICF induced genes in cell cycle categories and downregulated genes associated with metabolic processes. The Kyoto Encyclopedia of Genes and Genomes database revealed differentially regulated genes related to the p53 signaling pathway and cell cycle. q PCR analysis demonstrated significant upregulation of Ccnd1, Cdk6 and Ccng1. Flow cytometry showed that ICF induced cell cycle and proliferation, while reducing the number of apoptotic cells. ICF also upregulated transforming growth factor β1(Tgfb1) at both m RNA and protein levels, and pretreatment with a TGF-β inhibitor(SB431542) prior to ICF abolished ICF-induced Ccnd1 and Cdk6 expression. Taken together,these findings show that TGF-β signaling in i PSCs enhances proliferation and decreases apoptosis in response to ICF, that could give rise to an efficient protocol to manipulate i PSCs for organoid fabrication.

关键词： cycling culture attached

Long-term and non-invasive in vivo tracking of DiD dye-labeled human hepatic progenitors in chronic liver disease models

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World Journal of Hepatology 2022年第10期14卷 1884-1898页

作者： Chaturvedula Tripura Srinivas Gunda Sandeep Kumar Vishwakarma Avinash Raj Thatipalli Jedy Jose Mahesh Kumar Jerald Aleem Ahmed Khan Gopal Pande cell and stem cell biology CSIR-Centre for Cellular and Molecular BiologyHyderabad 500007TelanganaIndia Central Laboratory for stem cell research and Translational Medicine Centre for Liver Research and DiagnosticsDeccan College of Medical SciencesHyderabad 500058TelanganaIndia

BACKGROUND Chronic liver diseases(CLD)are the major public health burden due to the continuous increasing rate of global morbidity and mortality.The inherent limitations of organ transplantation have led to the development of stem cell-based therapy as a supportive and promising therapeutic option.However,identifying the fate of transplanted cells in vivo represents a crucial obstacle.AIM To evaluate the potential applicability of DiD dye as a cell labeling agent for longterm,and non-invasive in vivo tracking of transplanted cells in the liver.METHODS Magnetically sorted,epithelial cell adhesion molecule positive(1×106 cells/mL)fetal hepatic progenitor cells were labeled with DiD dye and transplanted into the livers of CLD-severe combined immunodeficiency(SCID)mice.Near-infrared(NIR)imaging was performed for in vivo tracking of the DiD-labeled transplanted cells along with colocalization of hepatic markers for up to 80 d.The existence of human cells within mouse livers was identified using Alu polymerase chain reaction and sequencing.RESULTS NIR fluorescence imaging of CLD-SCID mice showed a positive fluorescence signal of DiD at days 7,15,30,45,60,and 80 post-transplantation.Furthermore,positive staining of cytokeratin,c-Met,and albumin colocalizing with DiD fluorescence clearly demonstrated that the fluorescent signal of hepatic markers emerged from the DiD-labeled transplanted cells.Recovery of liver function was also observed with serum levels of glutamic-oxaloacetic transaminase,glutamate-pyruvate transaminase,and bilirubin.The detection of human-specific Alu sequence from the transplanted mouse livers provided evidence for the survival of transplanted cells at day 80.CONCLUSION DiD-labeling is promising for long-term and non-invasive in vivo cell tracking,and understanding the regenerative mechanisms incurred by the transplanted cells.

关键词： Chronic liver diseases cell transplantation cell tracking and imaging DiD Hepatic progenitors

Bone loss from Wnt inhibition mitigated by concurrent alendronate therapy

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Bone research 2018年第2期6卷 167-176页

作者： Babita Madan Mitchell J.McDonald Gabrielle E.Foxa Cassandra R.Diegel Bart O.Williams David M.Virshup Program in Cancer and stem cell biology Duke-NUS Medical School center for Cancer and cell biology and Program for Skeletal Disease and Tumor Microenvironment Van Andel Research Institute department of Pediatrics Duke University

Dysregulated Wnt signaling is associated with the pathogenesis of cancers, fibrosis, and vascular diseases. Inhibition of Wnt signaling has shown efficacy in various pre-clinical models of these disorders. One of the key challenges in developing targeted anti-cancer drugs is to balance efficacy with on-target toxicity. Given the crucial role Wnts play in the differentiation of osteoblasts and osteoclasts, acute inhibition of Wnt signaling is likely to affect bone homeostasis. In this study, we evaluated the skeletal effect of small molecule inhibitor of an o-acyl transferase porcupine（PORCN） that prevents Wnt signaling by blocking the secretion of all Wnts. Micro-computed tomography and histomorphometric evaluation revealed that the bones of mice treated with two structurally distinct PORCN inhibitors LGK974 and ETC-1922159（ETC-159） had loss-of-bone volume and density within 4 weeks of exposure. This decreased bone mass was associated with a significant increase in adipocytes within the bone marrow. Notably,simultaneous administration of a clinically approved anti-resorptive, alendronate, a member of the bisphosphonate family,mitigated loss-of-bone mass seen upon ETC-159 treatment by regulating activity of osteoclasts and blocking accumulation of bone marrow adipocytes. Our results support the addition of bone protective agents when treating patients with PORCN inhibitors.Mitigation of bone toxicity can extend the therapeutic utility of Wnt pathway inhibitors.

关键词： Wnt ETC Bone loss Wnt inhibition mitigated concurrent alendronate therapy

A highly efficient method for enriching TALEN or CRISPR/Cas9-edited mutant cells

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Journal of Genetics and Genomics 2016年第12期43卷 705-708页

作者： Hideyo Yasuda Eunsu Kim Abu Musa Md Talimur Reza Jin-Hoi Kim department of stem cell and Regenerative biology Konkuk University

In recent years,genome editing with site-specific nucleases,such as ZFN（zinc finger nuclease）,TALEN（transcription activatorlike effector nucleases）,and CRISPR/Cas9（the type II bacterial clustered,regularly interspaced,short palindromic repeats-associated protein 9）,has gained popularity for use in cell lines,animals,and plants（Urnov et al.,2010;Miller et al.,2011;Cong et al.

关键词： A highly efficient method for enriching TALEN or CRISPR/Cas9-edited mutant cells gene DNA RNA ZFN

Connecting past and present:single-cell lineage tracing

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Protein & cell 2022年第11期13卷 790-807页

作者： Cheng Chen Yuanxin Liao Guangdun Peng center for cell Lineage and Development CAS Key Laboratory of Regenerative BiologyGuangdong Provincial Key Laboratory of Stem Cell and Regenerative MedicineGIBH-HKU Guangdong-Hong Kong Stem Cell and Regenerative Medicine Research CentreGuangzhou Institutes of Biomedicine and HealthChinese Academy of SciencesGuangzhou 510530China center for cell Lineage and Atlas Bioland Laboratory(Guangzhou Regenerative Medicine and Health Guangdong Laboratory)Guangzhou 510005China Institute for stem cell and Regeneration Chinese Academy of SciencesBeijing 100101China University of Chinese Academy of Sciences Beijing 100049China

Central to the core principle of cell theory,depicting cells'history,state and fate is a fundamental goal in modern biology.By leveraging clonal analysis and sin-gle-cell RNA-seq technologies,single-cell lineage trac-ing provides new opportunities to interrogate both cell states and lineage histories.During the past few years,many strategies to achieve lineage tracing at single-cell resolution have been developed,and three of them(in-tegration barcodes,polylox barcodes,and CRISPR barcodes)are noteworthy as they are amenable in experimentally tractable systems.Although the above strategies have been demonstrated in animal develop-ment and stem cell research,much care and effort are still required to implement these methods.Here we review the development of single-cell lineage tracing,major characteristics of the cell barcoding strategies,applications,as well as technical considerations and limitations,providing a guide to choose or improve the single-cell barcoding lineage tracing.

关键词： single-cell lineage tracing integration barcodes polylox barcodes CRISPR barcodes

Pre-existing chromatin accessibility of switchable repressive compartment delineates cell plasticity

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National Science Review 2022年第6期9卷 100-113页

作者： Xiaolong Ma Xuan Cao Linying Zhu Ying Li Xuelong Wang Baihua Wu Gang Wei Lijian Hui State Key Laboratory of cell biology Shanghai Institute of Biochemistry and Cell Biology Center for Excellence in Molecular Cell Science Chinese Academy of Sciences School of Life Science and Technology Shanghai Tech University School of Life Science Hangzhou Institute for Advanced Study University of Chinese Academy of Sciences University of Chinese Academy of Sciences Bio-research Innovation center Shanghai Institute of Biochemistry and Cell Biology Institute for stem cell and Regeneration Chinese Academy of Sciences CAS Key Laboratory of Computational biology Shanghai Institute of Nutrition and Health Chinese Academy of SciencesUniversity of Chinese Academy of Sciences

cell plasticity endows differentiated cells with competence to be reprogrammed to other lineages. Although extrinsic factors driving cell-identity conversion have been extensively characterized, it remains elusive which intrinsic epigenetic attributes, including high-order chromatin organization, delineate cell plasticity.By analysing the transcription-factor-induced transdifferentiation from fibroblasts to hepatocytes, we uncovered contiguous compartment-switchable regions(CSRs) as a unique chromatin unit. Specifically,compartment B-to-A CSRs, enriched with hepatic genes, possessed a mosaic status of inactive chromatin and pre-existing and continuous accessibility in fibroblasts. Pre-existing accessibility enhanced the binding of inducible factor Foxa3, which triggered epigenetic activation and chromatin interaction as well as hepatic gene expression. Notably, these changes were restrained within B-to-A CSR boundaries that were defined by CTCF occupancy. Moreover, such chromatin organization and mosaic status were detectable in different cell types and involved in multiple reprogramming processes, suggesting an intrinsic chromatin attribute in understanding cell plasticity.

关键词： cell plasticity intrinsic properties compartment-switchable regions mosaic status pre-existing accessibility hepatic transdifferentiation

Neuroprotective properties of extracellular vesicles derived from mesenchymal stem cells

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Neural Regeneration research 2016年第6期11卷 904-905页

作者： akvile jarmalaviciūte augustas pivoriūnas department of stem cell biology State Research Institute Centre forInnovative Medicine Vilnius Lithuania

Extracellular vesicles（EVs）provide a novel mechanism of intercellular communication via the transfer of proteins,lipids,and miR NAs between cells.It is now widely accepted that cargo content of EVs depends on cell type and its physiological state.Accordingly,EVs derived from healthy cells may have a comparable therapeutic potential as cells themselves.

关键词： vesicles cargo intercellular physiological lipids comparable themselves notion neuronal displayed